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Biomedical subjects

James Cleary

Publications and source records attributed to James Cleary.

6 recordsLinked to original sources
PubMed2007

Effects of prayer and religious expression within computer support groups on women with breast cancer.

Research indicates that two common ways breast cancer patients or women with breast cancer cope with their diagnosis and subsequent treatments are participating in computer support groups and turning to religion. This study is the first we are aware of to examine how prayer and religious expression within computer support groups can contribute to improved psychosocial outcomes for this population. Surveys were administered before group access and then 4 months later. Message transcripts were analyzed using a word counting program that noted the percentage of words related to religious expression. Finally, messages were qualitatively reviewed to better understand results generated from the word counting program. As hypothesized, writing a higher percentage of religion words was associated with lower levels of negative emotions and higher levels of health self-efficacy and functional well-being, after controlling for patients' levels of religious beliefs. Given the proposed mechanisms for how these benefits occurred and a review of the support group transcripts, it appeared that several different religious coping methods were used such as putting trust in God about the course of their illness, believing in an afterlife and therefore being less afraid of death, finding blessings in their lives and appraising their cancer experience in a more constructive religious light.

Activities of Daily Living↗
PubMed2003

Prolactin modulates the naive B cell repertoire.

Prolactin is a peptide hormone produced by the anterior pituitary gland that is critical in lactation. Prolactin can also be produced by lymphocytes, and both B and T cells express prolactin receptors. These findings have suggested that prolactin has immunomodulatory functions. Studies in spontaneously autoimmune hosts have demonstrated a role for prolactin in augmenting autoreactivity. We chose to analyze prolactin effects on anti-DNA B cells in nonspontaneously autoimmune female BALB/c mice transgenic for the heavy chain of an anti-DNA antibody. Treatment with prolactin for 4 weeks induced a lupus-like phenotype with an increased number of transgene-expressing B cells, elevated serum anti-DNA antibody titers, and glomerular immunoglobulin deposits. Prolactin caused a decrease in the population of transitional B cells and an increase in mature follicular and marginal zone B cells. The DNA-reactive B cells had a follicular cell phenotype. Anti-DNA hybridomas demonstrated that prolactin alters selection of the naive B cell repertoire. The expansion and activation of anti-DNA B cells in prolactin-treated R4A-gamma2b BALB/c mice was dependent on the presence of CD4(+) T cells. Finally, treatment with prolactin was unable to break tolerance in R4A-gamma2b transgenic C57Bl/6 mice, suggesting that responsiveness of the immune system to prolactin is genetically determined.

Animals↗
PubMed2002

Treatment of pain crisis at end of life from severe lower extremity venous outflow obstruction with hyperalgesia and allodynia.

Pain crisis in metastatic disease can be a therapeutic dilemma when differing mechanisms contribute to severe hyperalgesia and neuropathic pain. We discuss clinical presentation and management of excruciating pain from severe lower limb venous outflow obstruction in an opioid tolerant, terminally ill patient with locally invasive and metastatic adenocarcinoma of the cervix. This case illustrates how pain crises at end of life can be successfully managed by using a rational, complementary, multimodal approach. Key points include possible mechanisms of pain from venous outflow obstruction, benefit of hyperbaric subarachnoid bupivacaine, opioid rotation to methadone, and use of ketamine by mouth.

Journal Article↗
PubMed2002

Estrogen alters thresholds for B cell apoptosis and activation.

Estrogen is thought to contribute to the increased frequency of autoimmune disorders occurring in females, but a molecular basis for its effects on autoimmunity remains to be elucidated. We have shown previously that estrogen leads to the survival and activation of autoreactive cells in the naive repertoire. To identify the molecular pathways involved in B cell tolerance, we sought to identify genes that are differentially regulated by estrogen in mouse B cells. Several genes involved in B cell activation and survival, including cd22, shp-1, bcl-2, and vcam-1, were upregulated by estrogen in B cells. We found that overexpression of CD22 and SHP-1 in B cells decreased B cell receptor signaling. Estrogen receptors alpha and beta are expressed on B cells and are functional, since they can directly upregulate expression of CD22, SHP-1, and Bcl-2. Estrogen treatment protected isolated primary B cells from B cell receptor-mediated apoptosis. These results suggest that estrogen induces a genetic program that alters survival and activation of B cells in a B cell-autonomous fashion and thus skews the naive immune system toward autoreactivity.

Animals↗