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Biomedical subjects

C Lane

Publications and source records attributed to C Lane.

At least 19 recordsLinked to original sources
PubMed1995

Development of a cervical cancer education program for native American women in North Carolina.

The North Carolina Native American Cervical Cancer Prevention Project is a five-year, NCI-funded public health education program. The project was developed to address the problem of excess mortality from cervical cancer among Native American women by increasing screening and follow-up of abnormal cervical smears. This paper describes the process of developing and implementing the intervention, an individualized health education program. Development of the intervention was guided by the health belief model, social learning theory, self efficacy theory, and PRECEDE, a planning model. Community analysis revealed that the target populations had limited awareness of cervical cancer as a specific type of cancer, and had an experientially-based pessimistic outlook regarding survival with cancer. Steps in developing the cervical-cancer prevention program included 1) development of objectives, 2) selection of strategies and development of cervical cancer education materials, 3) pretesting and revision, and 4) implementation, monitoring, and further revision. Native American lay health educators were recruited and trained to deliver the program. The experience of developing and implementing the individualized health education program suggests that the design of health education programs for Native Americans should begin with examination of basic assumptions regarding the nature of health and illness in the target population. The unique cultures and the diversity of Native American populations are critical factors in the development of health education programs for them.

Adolescent↗
PubMed1992

Induction of VCAM-1 and ICAM-1 on human neural cells and mechanisms of mononuclear leukocyte adherence.

We propose that leukocyte-derived cytokines induce the expression of adhesion molecules on the surface of neural cells that facilitates the subsequent attachment of leukocytes. Leukocyte adherence may contribute to some of the neural cell injury seen with various inflammatory diseases of the nervous system. With an in vitro model system, we have shown that mononuclear leukocytes bind to human neuroblastoma and cortical neuron cells only after the neural cells are stimulated with TNF-alpha. TNF-alpha stimulates expression of vascular cell adhesion molecule-1 (VCAM-1) in both of these neural cell lines. VCAM-1 mRNA is increased and VCAM-1 protein can be identified on the neural cell membranes with a new VCAM-1-specific mAb, CL40/2 F8. TNF-alpha also induces ICAM-1 in both of these neural cell lines. Leukocyte beta 1 (CD29) and beta 2 (CD18) integrins and their respective ligands, ICAM-1 and VCAM-1, on neural cells appear to be the dominant ligands mediating MNL:neural cell adhesive interactions. mAb to CD18 block 32 to 57% of the MNL binding to neural cells; similar inhibition is seen with mAb to ICAM-1. mAb to CD29 block 16 to 17% of the MNL binding to the neural cells suggesting that leukocyte beta 1 integrins and neural VCAM-1 may be a second route for MNL:neural cell interactions. Addition of both anti-CD18 and anti-CD29 mAb have an additive blocking effect; both ligand pairs may participate in MNL adhesion to neural cells, reminiscent of the multiplicity of ligands used by MNL when binding to endothelium.

Antibodies, Monoclonal↗
PubMed1992

How loss affects anger and alienates potential supporters.

The effects of loss of resources and illness symptoms on experienced anger, anger expression, and supporter's anger was studied among patients with severe chronic breathing disorder. Both illness symptoms and resource loss were related to greater anger. Angry feelings, in turn, led to more angry behavior. This angry behavior, in turn, resulted in increased anger of supporters. This process illustrates how chronic stress depletes both personal resources and social resources, making the individual increasingly vulnerable to further stressful experiences, inevitably to be confronted in chronic stress sequences.

Adaptation, Psychological↗
PubMed1992

Effect of an inhaled thromboxane mimetic (U46619) on in vivo pulmonary resistance and airway hyperresponsiveness in dogs.

1. We investigated the role of thromboxane A2 in the airway hyperresponsiveness that follows the inhalation of ozone in dogs by examining the responses to an inhaled thromboxane analogue (U46619). 2. Measurements of pulmonary resistance were made in anaesthetized dogs; the concentration of inhaled agonist causing an increase of 5 cmH2O l-1 s was calculated (provocative concentration). The effect of inhaled U46619 was studied on in vivo canine airway resistance, on airway responsiveness and on airways made hyperresponsive following the inhalation of ozone. 3. Inhaled thromboxane is a potent constrictor of the canine airway. The mean provocative concentration was 2.13 x 10(-4) M, compared to acetylcholine which was 3.23 x 10(-2) M. 4. Inhaled thromboxane did not result in the development of airway hyperresponsiveness to acetylcholine. Following U46619 inhalation the mean provocative concentration to acetylcholine was 3.92 x 10(-2) M. 5. Canine airway was not hyperresponsive to inhaled thromboxane following the inhalation of ozone. This was not due to an inhibition of acetylcholinesterase as the dogs were hyperresponsive to carbachol (a muscarinic agonist not degraded by endplate cholinesterase). 6. These experiments do not support a role for thromboxane in the development of airway hyperresponsiveness following the inhalation of ozone in dogs.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Anoxia/reoxygenation-induced neutrophil adherence to cultured endothelial cells.

Previous studies have shown enhanced neutrophil adhesion to endothelial cells exposed to anoxia and then reoxygenated (A/R). To define the molecular basis for these observations, we evaluated the relative roles of CD11/CD18 determinants (CD11a and CD11b) of neurtrophils and the endothelial adhesion proteins intercellular adhesion molecule 1 (ICAM-1) and endothelial-leukocyte adhesion molecule 1 (ELAM-1). Human umbilical vein endothelial cell (HUVEC) monolayers were exposed to anoxia for 30 min, reoxygenated, and then reacted with 51Cr-labeled neutrophils in adhesion assays. Neutrophil adhesion to HUVEC exposed to A/R was significantly increased (2.7-fold) as compared with that observed with normoxic (control) HUVEC. This A/R-induced hyperadherence was significantly diminished by monoclonal antibodies (MAb) directed at CD11a, CD11b, CD18 or ICAM-1, but not by MAb directed at ELAM-1. The inhibitory effects of anti-CD11a and anti-CD11b were additive and equivalent to that of anti-CD18 MAb. A/R did not elicit increased levels of ICAM-1 or ELAM-1 mRNA or surface protein. However, immunofluorescence flow cytometry indicated that incubation of neutrophils in supernatants of A/R-conditioned HUVEC elicited an increase of surface CD11b and CD18, but not CD11a. Supernatants from A/R-conditioned HUVEC promoted neutrophil adherence to naive HUVEC, and this hyperadhesivity was diminished by a platelet-activating factor (PAF) receptor antagonist and catalase but not by a 5-lipoxygenase inhibitor, a leukotriene B4 receptor antagonist, or superoxide dismutase. These studies indicate that A/R promotes neutrophil adherence via CD11a/CD18- and CD11b/CD18-dependent interactions with ICAM-1 that appear to be mediated by hydrogen peroxide and PAF.

Antibodies, Monoclonal↗
PubMed1991

Antibodies against human neutrophil LECAM-1 (LAM-1/Leu-8/DREG-56 antigen) and endothelial cell ELAM-1 inhibit a common CD18-independent adhesion pathway in vitro.

Neutrophil adhesion to interleukin-1 (IL-1)-stimulated human umbilical vein endothelial cells (HUVEC) involves the CD18 family of leukocyte integrins (lymphocyte function-associated antigen-1 [LFA-1], Mac-1, and p150,95) and LECAM-1 (DREG-56/LEU-8/LAM-1 antigen) on neutrophils and intercellular adhesion molecule-1 (ICAM-1) and endothelial leukocyte adhesion molecule-1 (ELAM-1) on the endothelium. In this study, we compare CD18-independent adhesion pathways mediated by neutrophil LECAM-1 and endothelial ELAM-1 and find that these two pathways overlap in a variety of assays: (1) anti-LECAM-1 and anti-ELAM-1 monoclonal antibody (MoAb) inhibit neutrophil binding to HUVEC, and the inhibitory effect is not additive; (2) anti-LECAM-1 MoAb, like anti-ELAM-1 MoAb, inhibits neutrophil binding to HUVEC stimulated for 3 hours with IL-1, but not to HUVEC stimulated for 8 hours, by which time ELAM-1 expression is downregulated; (3) anti-ELAM-1 MoAb has no effect on transendothelial migration, a CD18-dependent, LECAM-1-independent neutrophil function. Interestingly, anti-ELAM MoAb has a reduced but significant inhibitory effect on the adhesion of activated neutrophils that have shed their cell-surface LECAM-1. We also show that neutrophil binding to ELAM-1-transfected L cells is inhibited not only by anti-ELAM-1 but also by anti-LECAM-1 MoAb. These results suggest that LECAM-1 and ELAM-1 can operate in the same adhesion pathway, possibly as a receptor-counterreceptor pair. LECAM-1 and ELAM-1 are likely to interact with other ligands as well, perhaps through carbohydrate determinants that modify more than one glycoprotein.

Animals↗
PubMed1991

Development of two new monoclonal antibodies reactive to a surface antigen present on human ovarian epithelial cancer cells.

Monoclonal antibodies which bind selectively to cancer cells are currently used for tumor localization and for targeting cytotoxic reagents. The success of these approaches depends on the specificity of the antibody and its reactivity to a majority of the tumor samples. Frequently, monoclonal antibodies are generated by immunizing mice with antigenic preparations from a single tumor cell line. Antibodies generated under these conditions often react to a narrow range of tumors. In the present study, mice were immunized with multiple ovarian cancer cell lines in a sequential manner to amplify the immune response against common antigenic determinants expressed in these cell lines. Spleen cells from the immunized mice were then fused with NS-1 myeloma cells to establish hybridomas. Two cell lines were selected on the basis of their selective reactivity to ovarian cancer cells after extensive screening. Monoclonal antibodies OVX1 and OVX2 bound to all 5 ovarian carcinoma cell lines tested and did not bind to normal fibroblast cells. These antibodies recognized a unique antigenic determinant present in ovarian and breast cancer cells. Cross-blocking studies showed that the binding of OVX1 and OVX2 is not displaceable by 10 other previously described anti-ovarian antibodies including OC125. In immunocytochemical studies, OVX1 reacted to a majority of ovarian cancer tissues (17 of 20) and did not bind to normal ovarian tissues. Preliminary results indicate that OVX1 and OVX2 antibodies are directed to a high molecular weight antigen. These antibodies could be used in the preparation of cytotoxic conjugates.

Animals↗
PubMed1990

Inhibition of microvascular endothelial cell proliferation by vitreous following retinal scatter photocoagulation.

Laser photocoagulation of pig retina induced breakdown of the blood-retinal barrier, with the appearance of serum proteins in the vitreous as determined by sodium dodecyl sulphate/polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting techniques. Vitreous from lasered eyes inhibited the proliferation of cultured retinal microvascular endothelial cells in comparison with vitreous from non-lasered control eyes, and the inhibitory effect in the lasered eyes persisted for at least seven days. Inhibition was specific for endothelial cells, since no effect was observed when retinal pericytes or Tenon's fibroblasts were the target cells. These results suggest that indirect scatter photocoagulation may induce regression of neovascularisation by causing breakdown of the blood-retinal barrier and thus releasing into the vitreous serum components which result in inhibition of retinal microvascular endothelial cell growth.

Animals↗
PubMed1989

Cerebrospinal fluid quinolinic acid concentrations are increased in acquired immune deficiency syndrome.

Dementia and brain atrophy are established features of a large proportion of patients with acquired immune deficiency syndrome (AIDS). To investigate a potential mechanism for atrophy in AIDS, we measured the concentration of the endogenous neurotoxin quinolinic acid in the cerebrospinal fluid of 10 patients with AIDS and found that they had 3-fold higher quinolinic acid concentrations than 9 age-matched control subjects: 53.8 +/- 10.7 pmol/ml versus 18.4 +/- 3.4 pmol/ml, respectively (p less than 0.005). It remains to be determined whether increased brain quinolinic acid concentrations are involved in the pathogenesis of the neuropathology of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Transplantation of retinal pigment epithelium using a pars plana approach.

We describe a pars plana approach for transplantation of autologous retinal pigment epithelial cells from a peripheral chorioretinal biopsy to prepared Bruch's membrane at the posterior pole of the same eye. The technique has potential application in research and could be clinically applicable in the treatment of senile macular degeneration.

Animals↗
PubMed1988

Effects of vitreous from photocoagulated eyes on retinal microvascular cells in culture: a preliminary report.

Panretinal photocoagulation was carried out in mini pigs in an attempt to elucidate the mechanisms involved in laser therapy. The effect of the vitreous from these eyes on the proliferation of retinal microvascular endothelial cells was then studied. Vitreous removed 4 days after panretinal photocoagulation had no effect on the proliferation of bovine retinal microvascular endothelial cells in basal medium but inhibited proliferation in growth medium. Control vitreous was mitogenic for the microvascular cells in basal medium but this effect was not observed in growth medium.

Animals↗
PubMed1986

Stimulation and expansion of a human T-cell subpopulation by a monoclonal antibody to T-cell receptor molecule.

A murine monoclonal antibody (MAb) was obtained that showed unique specificity for the immunizing T-cell line HPB-ALL. This antibody, C37 (an IgG1,K) also reacted with a small (2-5%) population of normal peripheral blood T (PBL-T) cells. These C37-positive (C37+) cells were found in both the T4/Leu3+ and T8/Leu2+ subsets. Like OKT3 antibody, C37 induced T-cell mitogenesis with a peak proliferative response at day 3. In long-term cultures containing irradiated autologous feeder cells and IL-2, C37 antibody caused the selective expansion of C37+ T cells. On HPB-ALL cells C37 induced comodulation of the T3 molecule. C37 precipitated a disulfide-linked dimer characteristic of the T-cell antigen receptor consisting of an alpha-subunit (45-48 kD) and a beta-subunit (38-42 kD) from both C37+ T-cell blasts of a normal individual and HPB-ALL cells that were surface radioiodinated. However, the precipitated molecule isolated from C37 antibody-activated T-cell blasts exhibited a different pI from that isolated from HPB-ALL cells. Our studies indicate that C37 recognizes an epitope on the T-cell receptor molecule that is shared by a subpopulation of human T cells, which raises the possibility that multiple variable-region associated and/or framework-like determinants of the T-cell antigen receptor can be defined serologically and used in functional and molecular studies of T-cell subsets.

Antibodies, Monoclonal↗
PubMed1986

Therapy for the occupationally injured hand.

Basic considerations for rehabilitation of the occupationally injured hand are discussed. Factors affecting motivation of the patient as well as clinical assessment and treatment planning are reviewed. Brief postoperative routines for common injuries are outlined.

Carpal Tunnel Syndrome↗
PubMed1985

Biochemical characterization of a p43,12 complex: comparison with human and murine class I molecules.

A monoclonal antibody designated as C21 reacting with a p43,12 complex was developed against human thymocytes. It stained predominantly the early hematopoietic cells of the lymphoid lineage and also thymocytes, peripheral B-cells and activated T- and B-cells similarly to OKT10. The heavy chain of this antigen was a glycoprotein of Mr 43,000 (p43). Sequential immunoprecipitation with C21 and OKT10 antibodies indicated that they both reacted with an identical heavy-chain molecule. This observation was further documented by two-dimensional analysis. Monoclonal antibody C21 was used to probe a p43,12 complex further. Structural polymorphism of the p43 heavy chain isolated from T- and B-cells of different individuals was not detected by chymotryptic peptide mapping, although molecules from these cell types possessed a different charge on two-dimensional gels. An unusual observation was made regarding this complex on MOLT4 cells. The light chain co-precipitated from these cells was 12,000 daltons and had a pI distinct from that of beta 2-microglobulin but similar to the pI of the beta t molecule. Comparison between chymotryptic peptide maps of the p43 heavy chain and those of the human and murine class I molecules such as HLA, T6, H-2K, Qa-2 and TL revealed no apparent homology. We have shown, however, that the peptide backbone of p43, as studied by both tunicamycin treatment of cells and endoglycosidase F digestion of immunoprecipitates, was identical in size to that of murine Qa-1. These results suggest that the p43 antigen may be homologous to murine Qa-1 or another class I antigen encoded in the murine TL:Qa region.

Amino Acid Sequence↗