Biomedical subjects
Publications and source records attributed to M L Knapp.
Too many community needs assessments are taking too long, says this community health expert. To get projects under way, she offers the healthcare systems' model for resolving problems in a rapidly changing environment.
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Lipid peroxides were measured in cerebrospinal fluid (CSF) and sera from patients with multiple sclerosis (MS) or other conditions and from control subjects. In serum, visible fluorescence, A240nm, and free and protein-bound thiobarbituric acid (TBA)-reactive substances were significantly greater in MS patients than in control subjects. No such differences were observed in CSF. There was no correlation between lipid peroxides and disease severity or relapse time. We observed a significant positive correlation between CSF protein-bound TBA-reactive substances and CSF protein, suggesting that production of the former depends on protein concentration. A significant negative correlation between free TBA-reactive substances in serum and ultraviolet fluorescence indicated that production of free TBA-reactive substances may be associated with decreased production of fluorescent lipid peroxides. This study provides evidence for increased lipid peroxidation in serum but not CSF from MS patients, suggesting that either there is no increase in CSF lipid peroxidation in MS patients or that CSF lipid peroxides are rapidly removed, possibly by binding to CSF proteins that can be reabsorbed into the blood.
Fasting blood samples were collected from 83 patients with histologically proven breast cancer and analysed for plasma glucagon, serum immunoreactive tumour necrosis factor (TNF alpha), insulin, glucose, growth hormone, cortisol and TSH. Samples from patients with known diabetes mellitus or thyroid disease, and those on parenteral nutrition or with evidence of infection were excluded as were patients who had a history of weight loss through dieting or who were anorexic. Fasting plasma glucagon, serum cortisol and immunoreactive TNF alpha concentrations in patients with stage IV breast cancer who had developed weight loss were significantly higher than those in patients with stage IV disease who had not developed weight loss. There were no significant differences in the fasting serum concentrations of insulin, glucose, growth hormone and TSH between the two patient groups. The association between weight loss in stage IV breast cancer and increased concentrations of plasma glucagon, serum cortisol and TNF alpha suggests a possible role for these hormonal factors in the development of cancer cachexia.
Fasting venous blood collected from 83 patients with breast cancer was analyzed for triglycerides; total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol; tumor necrosis factor (TNF alpha); glucose; creatinine; insulin; glucagon; growth hormone; cortisol; and thyrotropin. Patients with stage IV disease had significantly higher (P less than 0.05) triglyceride concentrations and significantly lower (P less than 0.05) concentrations of total and HDL cholesterol than did patients with less advanced disease or age-matched controls. Furthermore, LDL cholesterol concentrations in patients with boney metastases were significantly lower (P less than 0.05) than concentrations in patients with liver or liver plus boney metastases or in controls. These results could not be attributed to smoking habits, alcohol consumption, or treatment. We observed no correlations between serum concentrations of lipid and concentrations of TNF alpha, insulin, glucose, creatinine, cortisol, growth hormone, or thyrotropin. However, there was a significant (P less than 0.05) negative correlation between total cholesterol and glucagon and between LDL cholesterol and glucagon for patients with stage II, III, and IV disease, suggesting that glucagon may reduce LDL cholesterol concentrations by an as-yet-unidentified mechanism.
Plasma samples from patients attending a lipid clinic (n = 14) and healthy control subjects (n = 21) were assayed for fibrinogen using an immunochemical method (radial immunodiffusion) and a turbidimetric assay based on the thrombin clotting technique. The patients had significantly higher plasma fibrinogen concentrations than controls by both methods, but there was significant overlap between the two groups when fibrinogen was assayed by the thrombin clotting technique; there was almost complete separation of the two groups using the immunochemical assay. This difference in overlap could not be attributed to the presence or absence of fibrinogen degradation products. These findings may have important implications for the choice of method for determining plasma fibrinogen when assays are used for the assessment of cardiovascular risk. It is recommended that plasma fibrinogen should be assayed by both an immuno-chemical and a thrombin clotting method.
A radioimmunoassay for the measurement of gonadotrophin releasing hormone (GnRH) in plasma and urine using readily available reagents was developed. The GnRH assay showed good precision, recovery, and parallelism over a wide range of GnRH concentrations with a sensitivity of 15 pg/ml. The assay was compared with a commercially available kit (Buhlmann Laboratories). Although the Buhlmann kit showed acceptable precision, recovery, sensitivity, and correlation with the developed GnRH assay for plasma samples, lack of parallelism of serially diluted plasma and urine samples was consistently observed, together with a poor correlation with the developed GnRH assay for urine, suggesting a matrix effect with the Buhlmann kit. The developed assay is suitable for measuring GnRH in samples obtained from patients receiving pulsatile infusions of GnRH. In contrast, the commercially available Buhlmann kit was unsuitable for measuring plasma GnRH as the kit had a top standard of only 160 pg/ml, well below the peak plasma concentration. It would not be possible to dilute samples for analysis because of the lack of parallelism of diluted samples compared with standards obtained with the Buhlmann assay.
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The effects of heat treatment of serum samples on the hormone analyses used in this laboratory were studied. Total T4, testosterone, progesterone, and growth hormone were not systematically affected by heat treatment over the whole range of analyte concentrations studied; for thyroid stimulating hormone, no effect was noted on serum samples with concentrations of less than 10 mU/l. Significant changes occurred in total T3, cortisol, follicle stimulating hormone, luteinizing hormone, and prolactin. It is suggested that with appropriate preliminary study, heat treated plasma samples may be used in endocrinological investigations without adversely affecting the diagnostic validity of the results.
Negative interference by jaundiced plasma in kinetic Jaffé methods for plasma creatinine determination is caused by both conjugated and unconjugated bilirubin. The amount of interference observed is method- and temperature-dependent and is directly related to bilirubin concentration but is independent of the creatinine concentration. Bilirubin also significantly reduces the precision of the creatinine estimation. A mechanism of bilirubin interference in kinetic Jaffé methods is proposed and the influence of picrate concentration, hydroxide concentration and temperature on the magnitude of bilirubin interference has been investigated.
The non-dialysable fraction of haemolysate causes an apparent reduction of plasma alkaline phosphatase (ALP) activity using 4-nitrophenylphosphate as substrate. Analyses using four different buffers showed that the decrease in enzyme activity is affected by the buffer used. The percentage reduction in ALP activity is dependent on the initial ALP activity but not on the isoenzyme present. When diethanolamine was used as buffer, sample blanking almost completely compensated for the apparent reduction in enzyme activity. However, when aminomethylpropanol, aminomethylpropanediol and tris-carbonate buffers were used, it appeared that haemolysate reduced the catalytic activity of the enzyme, since sample blank correction had minimal effect on the results.
In a series of 47 patients with colorectal cancer, early-stage lesions were detected more frequently on routine screening than on symptomatic screening. Signs and symptoms tended to occur in combination rather than singly. Guaiac positivity was the sole sign in only one patient. Physicians must consider the possibility of colorectal cancer in patients with suggestive signs or symptoms.
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An oncofetal pancreatic antigen (OPA) has been identified and purified from the blood of patients with pancreatic cancer. Characterisation studies on OPA have shown that it is a protein of molecular weight 40 000 with alpha2 electrophoretic mobility. OPA is clearly different from alpha-fetoprotein, carcinoembryonic antigen, ferritin, acute phase reactants, and normal serum proteins. A rocket immunoassay has been developed allowing the quantitation of OPA in serum; it has been applied to samples from over 700 individuals with a variety of conditions. Elevated levels of OPA have been found in 42 of 48 (88%) patients with biopsy-proven pancreatic cancer and in a much smaller percentage of patients with other cancers or with other conditions considered in the differential diagnosis of pancreatic cancer. The studies indicate that serum OPA measurements may be useful as a preliminary screening test for pancreatic cancer and for monitoring the course of the disease.
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Pancreatic oncofoetal antigen (POA) has been isolated by affinity chromatography and used to standardise an immunoassay. POA was detected in foetal serum and in 97% of sera from 75 patients with carcinoma of the pancreas. Raised levels were also found in 16% of sera from 43 patients with chronic pancreatitis and in 3 of 156 patients with related conditions. Using an immunoperoxidase method, POA was regularly found in the foetal pancreas and in adult carcinoma of the pancreas. Weak staining was found in the foetal pancreas and in adult carcinoma of the pancreas. Weak staining was found in one carcinoma of the colon. Antisera from two other groups (Gelder and Moossa; Arndt and Thiele) react with the same antigenic moiety as does our anti-POA.