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R Turnage

Publications and source records attributed to R Turnage.

6 recordsLinked to original sources

Cell column chromatography: a new research tool to quantify cerebral cell volume changes following chemically-induced anoxia/re-oxygenation.

OBJECTIVE: The roles of individual types of cerebral cells in contributing to brain edema are undefined. The objective of this study was to determine the role of cerebral cell-column chromatography in quantifying cell volumes of individual cerebral cell lines, under chemically-induced anoxia/re-oxygenation (A/R). METHODS: Cerebral endothelial cells (4 experiments) or type II astrocytes (4 experiments) were cultured to confluence on microcarrier beads. A chromatographic cell-column of 1.5 cm height was filled with non-treated cell-covered beads. The column was perfused at 1 ml/min with a balanced perfusate for one hour (Baseline). The perfusate was then switched to that containing 5 mM thioglycolic acid for one hour (Anoxia). Then the column was perfused with the normal perfusate for another two hours (Re-oxygenation). The total free space in the column, reversely reflecting cell volumes, was determined by averaged transit time (TTa) of a non-permeable flow tracer blue dextran. Decreased TTa means that cells swell, and vice versa. RESULTS: TTa in endothelial cell columns increased with a peak at 60 minutes of re-oxygenation. TTa in astrocyte columns decreased with a nadir at 30 minutes of re-oxygenation. CONCLUSION: Cell column chromatography can be used to determine the cerebral cell volume changes following chemically-induced anoxia/re-oxygenation.

Brain Edema↗

Ifenprodil treatment is associated with a down-regulation of brain aquaporin 4 following cardiac arrest in rats.

OBJECTIVES: Ifenprodil, a NMDA receptor polyamine site antagonist, reduces experimental cardiac arrest (CA)-elicited brain edema, which is associated with an up-regulation of aquaporin 4 (AQP4), a brain water-selective channel. However, the interacting roles of NMDA receptors and AQP4 in CA-elicited brain edema are unknown. The objective of this study was to test our hypothesis that ifenprodil treatment is associated with a down-regulation of brain AQP4. METHODS: Twenty-five rats were assigned to normal controls (group 1, n = 6) or subjected to eight minutes of asphyxial CA treated with placebo (group 2, n = 9) or ifenprodil (group 3, n = 10). Ifenprodil at 10 mg/kg or normal saline of equal volume was given intraperitoneally, 5 minutes before CA. The density of AQP4 protein and actin bands was scanned and expressed as the ratios of the optical density of AQP4 relative to that of actin. The ANOVA analysis was used to compare the group differences. RESULTS: The ratios of the optical density of AQP4 to that of actin were 0.88 +/- 0.06 in group 1, 1.11 +/- 0.08 in group 2 (p < 0.05 vs. group 1), and 0.78 +/- 0.04 in group 3 (p < 0.01 vs. group 2; NS vs. group 1). CONCLUSION: Ifenprodil given before CA is associated with a downregulation of brain AQP4 in rats.

Animals↗

Primary colonic lymphoma.

BACKGROUND AND OBJECTIVES: The colon is a rare location for gastrointestinal non-Hodgkin's lymphoma (NHL). This study was undertaken to identify risk factors, presentation, treatment, and prognosis for primary colonic lymphoma (PCL) through review of a large tertiary care hospital system experience. METHODS: A retrospective review of all patients with colonic malignancy and NHL was performed using pathology and cancer registry databases from January 1989 to December 1998. Criteria for inclusion were no evidence of extraperitoneal disease, no leukemic or lymphomatous abnormalities in the blood, and disease confined to the colon. RESULTS: Seven patients met the inclusion criteria (4 male, 3 female; 33-72 years). They represented 1.4% of all NHL, 14% of gastrointestinal NHL and 0.9% of all colonic malignancies diagnosed during this period. Three of the patients had positive serology for human immunodeficiency virus; one was taking steroids chronically for Addison disease. The most common presentation was nonspecific abdominal pain. The lack of specific symptoms delayed diagnosis from 1-12 months. All patients underwent laparotomy with resection. The most common tumor location was the cecum (5/7, 71%). Regional lymph nodes were affected in all but 1 patient. All tumors were B-cell lymphomas (5 small noncleaved cell, 2 large cell). Six of 7 patients received adjuvant chemotherapy. Of the 6 patients available for follow-up four remain alive (12, 19, 23, and 25 months after diagnosis). In both patients who died the disease recurred diffusely. CONCLUSIONS: The colon is a rare location for NHL. Immunosuppression is the most common risk factor. Patients' frequently present with non-specific abdominal pain, this leads to lengthy delays in diagnosis. Most of these tumors are located in the cecal area. Surgery is the most widely utilized form of therapy. Although adjuvant therapy is frequently utilized, its' impact on survival is unclear.

Academic Medical Centers↗

Platelet activating factor (PAF) stimulates release of PGI2 from inflamed rabbit gallbladder cell cultures.

This study examines the hypothesis that PAF stimulates release of PGI2 from inflamed rabbit gallbladder explant cell cultures. New Zealand white rabbits underwent bile duct ligation for 72 h (72 h BDL), or sham operation, Sham and 72 h BDL gallbladder explants were placed in culture, and the cells grown to 75% confluence. The cells were exposed to increasing concentrations of PAF for 60 min. The media analyzed for eicosanoid release by EIA and the cells analyzed for cyclooxygenase and prostacyclin synthase content by immunoblot analysis. PAF increased release of 6-keto-PGF1 alpha from the 72 h BDL gallbladder cell cultures in a dose-related manner which was inhibited by indomethacin preincubation by 90%. The increased 72 h BDL cell release of 6-keto-PGF1 alpha was not associated with changes in the content of cyclooxygenase or prostacyclin synthase. PAF did not alter eicosanoid release from sham control cell cultures. These data suggest that PAF can only up-regulate endogenous 6-keto-PGF1 alpha release from the 72 h BDL cells that had been previously stimulated by inflammation. PAF may thus contribute to gallbladder distention and injury by chronic stimulation of inflamed gallbladder PGI2 release.

6-Ketoprostaglandin F1 alpha↗

A submucosal antral mass caused by cytomegalovirus infection in a patient with acquired immunodeficiency syndrome.

A 29-yr-old homosexual man with acquired immunodeficiency syndrome presented with watery diarrhea and fever. Upper gastrointestinal endoscopy was performed to obtain duodenal aspirates and biopsies. A 4-cm submucosal mass in the gastric antrum was identified. Subsequent abdominal CT scan confirmed the presence of this antral mass. An attempt at CT guided needle biopsy was nondiagnostic. Because the mass possibly represented a Kaposi's sarcoma or lymphoma, exploratory laparotomy and open biopsy was performed. Examination of the biopsy specimen showed inflammatory debris with multiple intranuclear cytomegalovirus inclusions. This report describes a case of a submucosal antral mass caused by localized cytomegalovirus infection in a patient with acquired immunodeficiency syndrome.

Acquired Immunodeficiency Syndrome↗

The effect of treatment for colorectal cancer on long-term health-related quality of life.

BACKGROUND: Little information is available on the impact that therapies used in the treatment of colorectal cancer (CRC) have on long-term, health-related quality of life (HRQL). Knowledge of how HRQL is affected by these therapies is essential in properly selecting patients for treatment. The purpose of this study was to determine the long-term impact that surgical and adjuvant therapy for resectable CRC has on patient-reported HRQL in a male veteran population through a case-control design. METHODS: All participating patients had completed therapy at least 6 months before enrollment. One hundred fifty-eight patients were accrued over a 3-year period (January 1, 1997 to December 31, 1999) at a single institution. The impact of CRC surgery on HRQL was measured by comparing a cohort of 61 patients undergoing surgery alone for the treatment of CRC (CRC-S group) with 44 patients undergoing surgery for benign colonic disease (BCD group). To study the effect of adjuvant therapy for CRC on HRQL, a third cohort of 53 patients undergoing both surgical and adjuvant treatment (CRC-S/A group) was compared with the CRC-S group. For each group, health status was measured by a health survey questionnaire, SHORT FORM 36 (SF36). For patients treated for CRC, an additional disease-specific supplemental questionnaire also was used. RESULTS: Self-reported health status, as measured by mean SF36 score, was significantly reduced for the BCD group compared with CRC-S patients on general health perception (41.9 +/- 3.9 vs. 52.2 +/- 3.0, P = .04) and the standardized physical component score (31.2 +/- 1.7 vs. 37.5 +/- 1.5, P < .005). Despite an increased number of distally located tumors, later stage cancers, and an increased number of recurrences in the CRC-S/A group compared with the CRC-S cohort, no significant differences were identified between these groups on any of the subscales or standardized scores of SF36. Using the supplemental questions, no differences were identified between the CRC groups with respect to appetite, weight, or gastrointestinal or urinary functioning. CONCLUSIONS: Surgical therapy for CRC probably has minimal impact on long-term HRQL when compared with surgery for benign colonic processes. Similarly, there does not appear to be a measurable, lasting impact of CRC adjuvant therapy on HRQL when compared with surgery alone. Although overall impact of therapies for CRC on HRQL appears to be limited, measurement of therapeutic influence on an individual level and identification of selection criteria based on estimated impact on HRQL for these therapies requires prospective validation.

Adult↗