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Biomedical subjects

B S Harrison

Publications and source records attributed to B S Harrison.

8 recordsLinked to original sources
PubMed1994

Colon cancer in blacks: age-related presentation and survival within a similar socioeconomic group.

Young blacks with colon cancer continue to have a poor survival rate for reasons that remain undetermined. Medical records of blacks with colon cancer diagnosed at an inner-city hospital during a 10-year period were reviewed. The cohort consisted of 118 indigent, nonmigratory patients grouped by age. Group 1 consisted of 11 patients under age 50, and group 2 consisted of 107 patients age 50 and over. Admission symptoms were significantly different between groups. Patients in group 1 presented with abdominal pain more often than patients in group 2, and none of the patients in group 1 had anemia or obstruction, which comprised 14% and 11%, respectively, of the presenting symptoms in group 2 patients. Overall, survival difference was significant; the survival rate was 22.8 months for group 1 and 64.2 months for group 2 (P < .02). There was no difference in stage at presentation to account for the decreased survival in group 1. It is possible that the overwhelming majority (45%) of patients in group 1 with abdominal pain actually had more virulent disease, which accounts for the short survival. These individuals must be targeted for more aggressive patient education, surveillance, early detection and treatment, and follow-up.

Adult↗
PubMed1991

Correlation of preoperative factors, severity of disease, type of oxygenator and perfusion times with mortality and morbidity of coronary bypass.

Previous studies have related preoperative status and severity of disease to the outcome of coronary artery bypass surgery. Although increased perfusion and clamp times increase the risk of cardiac surgical procedures, the importance of these factors in relation to the patient's preoperative condition and the severity of disease has not previously been determined. In this study of 1078 patients, we examined the correlation between the patient's preoperative condition, the severity of coronary disease, and duration of perfusion and clamp time, and the type of oxygenator used with the mortality and morbidity associated with coronary artery bypass grafting. One-way analysis of variance and multiple correlation analysis showed that perfusion time, clamp time and nonclamp perfusion time correlated with mortality, perioperative infarction, the use of intra-aortic balloon pump, stroke, renal failure, pulmonary failure, infection, and leg wound complications (p less than 0.05). Perfusion time, clamp time and nonclamp perfusion time did not correlate with postoperative bleeding or sternal wound complications. Nonclamp perfusion time correlated more strongly than any other factor with mortality, perioperative infarction, the use of intra-aortic balloon pump, renal failure, pulmonary failure and infection (p less than 0.05). Clamp time correlated more than any other factor with the development of leg-wound complications (p less than 0.05). The use of a bubble rather than a membrane oxygenator was significantly related to mortality, stroke, infection and leg wound complications by one-way analysis of variance (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

L-alpha-phosphatidylcholine-induced stimulation of PGI2 production in canine gallbladders following hypovolemic shock and Escherichia coli sepsis.

In vitro production of PGI2 in canine gallbladders subjected to hypovolemic shock and Escherichia coli sepsis was studied to determine whether a precursor above arachidonic acid in the cyclooxyenase cascade might be operative in the production of prostacyclin, which, in turn, may play a role in the pathogenesis of acute acalculous cholecystitis (AC). L-alpha-phosphatidylcholine (LaP), an arachidonic acid precursor, was used as the test agent. LaP did not stimulate PGI2 production from either gallbladder surface in the hypovelimic animals or the mucosa of the septic shock group. However, it did stimulate PGI2 production from the SS serosa compared with controls, 1375 +/- 432 versus 633 +/- 198 pg/cm2/min (P less than .05). In conclusion, lack of stimulation of PGI2 in the hypovolemic model suggests that PGI2 does not play a role in AC. Alternatively, it may play a role in preventing this disease process in septic shock. This study demonstrates the use of precursors of arachidonic acid and the cyclooxygenase pathway as active participants in the production of PGI2, although it is unclear whether the prostacyclin produced helps prevent AC in septic shock.

Acute Disease↗
PubMed1990

Decrease in cyclosporin-mediated prostacyclin production in renal versus carotid arteries: a mechanism for cyclosporin-induced hypertension.

Although the mechanism of cyclosporin (CsA)-induced hypertension is unknown, it has been shown to inhibit prostacyclin (PGI2) production directly, which may be a factor. We determined whether CsA had a differential effect on PGI2 production from the carotid artery (CA) and internal jugular vein (JV) compared to that from the renal artery (RA) and vein (RV) as a possible contributing factor to renovascular hypertension based upon the ability of organs to regulate their own blood flow according to local circumstances. The neck and renal vessels were removed from anesthetized adult female dogs (N = 8) and placed in a stimulation chamber, with Cell I being control (Hepes buffer), Cell II containing 0.3 mg/ml CsA, and Cell III containing CsA and 25 microM arachidonic acid (AA). Following serial stimulation periods, the supernatant was evaluated for PGI2 production by radioimmunoassay. PGI2 production from CA was significantly higher than that from RA following control and AA stimulation, 1474 +/- 382 pg/cm2-min vs 733 +/- 173 pg/cm2-min (P less than 0.05) and 2236 +/- 347 vs 1090 +/- 217 (P less than 0.01), respectively. CsA-induced PGI2 production from the carotid arteries was significantly greater than that from the renal arteries, 2944 +/- 586 vs 1003 +/- 235 (P less than 0.005). However, stimulation with AA following CsA resulted in sustained PGI2 production in both arteries that was similar to stimulation with CsA alone, 3014 +/- 600 vs 2944 +/- 586 for the carotids and 1278 +/- 280 vs 1003 +/- 235 for the renal arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗