Metabolism of baicalin by different microbiota determined by MimiCol.

Substances metabolised by the intestinal microbiota can be used as colon markers and are gaining importance. The flavonoid glycoside baicalin has been described in the literature to be metabolised by the intestinal microbiota. The aim of this work was to investigate how the biotransformation of baicalin to baicalein is related to the intestinal microbiota. For this purpose, stool samples from healthy volunteers with different dietary habits were used. From the pre-cultured stool samples, different standard microbiota were obtained which were used for the subsequent metabolism studies in the in vitro model MimiCol. MimiCol represents the ascending section of the colon, the colon ascendens, in terms of available volume, pH-value, redox potential and bacterial abundance. While during the experiments with added standard microbiota a metabolism of baicalin to baicalein could be detected, this was not the case in a series of experiments without added microbiota. This confirmed the hypothesis that the metabolism of baicalin relies on the bacterial species that are present in the colon. The data collected in the MimiCol therefore support the use of baicalin as a potential marker for the determination of the colon arrival. This can be explained by the fact that baicalin in its native form is poorly absorbed from the gastrointestinal tract. Enzymes of the colonic microbiota, namely ß-glucuronidases, hydrolyze baicalin to the aglycone baicalein. The resulting aglycone can be absorbed through the intestinal mucosa and detected in blood plasma. This potentially enables the use of baicalin as a marker to determine the time of arrival in the colon.

Dietary practices in pyridoxine non-responsive homocystinuria: a European survey.

BACKGROUND: Within Europe, the management of pyridoxine (B6) non-responsive homocystinuria (HCU) may vary but there is limited knowledge about treatment practice. AIM: A comparison of dietetic management practices of patients with B6 non-responsive HCU in European centres. METHODS: A cross-sectional audit by questionnaire was completed by 29 inherited metabolic disorder (IMD) centres: (14 UK, 5 Germany, 3 Netherlands, 2 Switzerland, 2 Portugal, 1 France, 1 Norway, 1 Belgium). RESULTS: 181 patients (73% >16 years of age) with HCU were identified. The majority (66%; n=119) were on dietary treatment (1-10 years, 90%; 11-16 years, 82%; and >16 years, 58%) with or without betaine and 34% (n=62) were on betaine alone. The median natural protein intake (g/day) on diet only was, by age: 1-10 years, 12 g; 11-16 years, 11 g; and >16 years, 45 g. With diet and betaine, median natural protein intake (g/day) by age was: 1-10 years, 13 g; 11-16 years, 20 g; and >16 years, 38 g. Fifty-two percent (n=15) of centres allocated natural protein by calculating methionine rather than a protein exchange system. A methionine-free l-amino acid supplement was prescribed for 86% of diet treated patients. Fifty-two percent of centres recommended cystine supplements for low plasma concentrations. Target treatment concentrations for homocystine/homocysteine (free/total) and frequency of biochemical monitoring varied. CONCLUSION: In B6 non-responsive HCU the prescription of dietary restriction by IMD centres declined with age, potentially associated with poor adherence in older patients. Inconsistencies in biochemical monitoring and treatment indicate the need for international consensus guidelines.

Critical analysis of a computer-assisted tutorial on ECG interpretation and its ability to determine competency.

BACKGROUND: We developed a computer-based tutorial and a posttest on ECG interpretation for training residents and determining competency. METHODS: Forty residents, 6 cardiology fellows, and 4 experienced physicians participated. The tutorial emphasized recognition and understanding of abnormal ECG features. Active learning was promoted by asking questions prior to the discussion of ECGs. Interactivity was facilitated by providing rapid and in-depth rationale for correct answers. Responses to questions were recorded and extensively analyzed to determine the quality of questions, baseline knowledge at different levels of training and improvement of grades in posttest. Posttest grades were used to assess improvement and to determine competency. RESULTS: The questions were found to be challenging, fair, appropriate and discriminative. This was important since the quality of Socratic questions is critical for the success of interactive programs. The information on strengths and weakness in baseline knowledge at different levels of training were used to adapt our training program to the needs of residents. The posttest revealed that the tutorial contributed to marked improvement in feature recognition. Competency testing distinguished between residents with outstanding grades and those who needed remediation. CONCLUSIONS: The strategy for critical evaluation of our computer program could be applied to any computer-based educational program, regardless of topic.

The role of platelet membrane phospholipids in the platelet release reaction.

The structure and function of the platelet surface was probed by phospholipase C (Clostridium perfringens) which hydrolyzes membrane phospholipids, particularly phosphatidylcholine. Platelet phospholipids were susceptible to phospholipase C, and extent of hydrolysis was dependent on concentration of phospholipase C and Ca(++). Phospholipase C (0.15 U/ml) with Ca(++) (0.55 mM) hydrolyzed 15.6% phospholipids during 5 min. Phospholipase C released platelet serotonin (5HT), ADP, and platelet factor 4. Hydrolysis of 5% phospholipids resulted in release of 70% 5HT. Platelet 5HT release was rapid, occurring within 2 min. Phospholipase C (0.2 U/ml) with Ca(++) (0.55 mM) also released 10.35 nmol sotrage pool ADP/10(9) platelets and 63% platelet factor 4 during 3 min. Phospholipase C did not cause leakage of cytoplasmic metabolic pool ADP, since only 6.6% [(3)H]ADP was released. Ultrastructural analysis of phospholipase C-modified platelets showed that platelets were intact. After 2% phospholipid hydrolysis, centralization of granules and contraction of microtubules were evident. After 18% phospholipid hydrolysis, there were morphological indications of degranulation. Phospholipase C-induced phospholipid hydrolysis caused the release of ADP and 5HT since: (a) Phospholipase C purified by heating was shown to be free of protease and neuraminidase activity and capable of inducing the platelet release reaction. (b) Antitoxin (Cl. perfringens) neutralized phospholipase C-induced 5HT release which rules out a contaminant. (c) Phosphorylcholine, the hydrolysis product, did not induce platelet 5HT release. This study demonstrates that minimal hydrolysis of platelet phospholipids triggers the release reaction. Our hypothesis is that phospholipids, presumably phosphatidylcholine, are situated at or near active site or "receptor" on the platelet surface and function as the modulator for the release reaction.

Biosynthesis of factor V in isolated guinea pig megakaryocytes.

Although platelets contain Factor V, localized primarily in the alpha-granules, the origin of this coagulation cofactor in these cells is not known. We therefore explored whether isolated megakaryocytes could biosynthesize Factor V. Guinea pig plasma Factor V coagulant activity was demonstrated to be neutralized by human monoclonal and rabbit polyclonal antibodies directed monospecifically against human Factor V. These antibodies had been used earlier to purify human Factor V. These antibodies had been used earlier to purify human Factor V and to quantify Factor V antigen concentration, respectively (1983. Chiu, H. C., E. Whitaker, and R. W. Colman. J. Clin. Invest. 72:493-503). As determined by a competitive enzyme-linked immunosorbent assay with guinea pig plasma as a standard, Factor V solubilized from guinea pig megakaryocytes was present at 0.098 +/- 0.018 micrograms/10(5) cells. Each megakaryocyte contained about 500 times as much Factor V as is in a platelet (0.234 +/- 0.180 micrograms/10(8) platelets). The content of Factor V antigen in guinea pig plasma was greater (27.0 +/- 3.0 micrograms/ml) than that of Factor V antigen in human plasma (11.1 +/- 0.4 micrograms/ml). In contrast, human platelets contain ninefold more Factor V antigen (2.01 +/- 1.09 micrograms/10(8) platelets) than do guinea pig were 2.85 +/- 0.30 U/ml plasma, 0.022 +/- 0.012 U/10(8) platelets, and 0.032 +/- 0.03 U/10(5) megakaryocytes, compared with human values of 0.98 +/- 0.02 U/ml plasma and 0.124 +/- 0.064 U/10(8) platelets. Isolated megakaryocytes were found to contain Factor V by cytoimmunofluorescence. The megakaryocytes were incubated with [35S]methionine, and radiolabeled intracellular proteins purified were on a human anti-Factor V immunoaffinity column. The purified protein exhibited Factor V coagulant activity and neutralized the inhibitory activity of a rabbit antihuman Factor V antibody, which suggests that megakaryocyte Factor V is functionally and antigenically intact. These results indicate that Factor V is synthesized by guinea pig megakaryocytes. Nonetheless, megakaryocyte Factor V was more slowly activated by thrombin and in the absence of calcium was more stable after activation than was plasma Factor Va. Electrophoresis in sodium dodecyl sulfate and autoradiography of the purified molecule showed a major band of Mr 380,000 and a minor band of Mr 350,000, as compared with guinea pig and human plasma Factor V, where the protein had an Mr of 350,000. Both forms of Factor V were substrates for thrombin. Possible explanations for the higher molecular weight and different thrombin sensitivity and stability observed are that a precursor of Factor V was isolated or that the megakaryocyte Factor V had not been fully processed before isolation.

Location of phosphatidylethanolamine and phosphatidylserine in the human platelet plasma membrane.

The location of phospholipids in the human platelet plasma membrane was probed with 2, 4, 6-trinitrobenzenesulfonate (TNBS). TNBS does not penetrate inintact cells and can label phosphatidylethanolamine (PE) and phosphatidylserine (PS). In tact platelets, PE is not accessible to TNBS during the initial 15 min. However, 6.9% PE reacts with TNBS after 30 min and 17.9% PE is labeled after 90 min. In intact platelets, PS is not labeled even after 2 h. In contrast, in phospholipids extracted from platelets 71% PE and 26.5% PS react with TNBS within 5 min. This indicates that PS is inaccessible and PE is relatively inaccessible to TNBS in intact platelets. After incubation of platelets with thrombin, there is increased labeling of PE but no labeling of PS. The incubation of platelets with thrombin (0.05 U/ml) for 5 min results in 16.2% increase of PE labeling during subsequent 30-min incubation with TNBS. PS does not appear to be a component of the functional surface of platelets. However, exposure of PE may have a critical role in platelet hemostatic function. The implication of the study is that there is asymmetry of phopholipids in the platelet plasma membrane which has considerable physiological significance.

Mediation of cytotoxic immune responses against human tumor-associated antigens by allogeneic immune RNA.

Allogeneic immune RNA (I-RNA), extracted from the peripheral blood lymphocytes of patients putatively cured of cancer, mediated cytotoxic immune reactions that apparently were directed specifically against human tumor-associated antigens. I-RNA was extracted from the peripheral blood lymphocytes of patients with various types of cancer. Patients selected had not been previously sensitized to HL-A or other normal transplantation antigens or to blood group antigens. Normal human peripheral blood lymphocytes were incubated with these allogeneic I-RNA preparations and tested for cytotoxicity against human target cells in vitro. Allogeneic I-RNA mediated cytotoxic immune reactions only against tumor target cells of the same histologic type as the I-RNA donor. I-RNA's extracted from peripheral blood lymphocytes of melanoma patients mediated cytotoxic immune reactions only against melanoma cells. Similarly, only I-RNA's extracted from the lymphocytes of patients with colon cancer mediated cytotoxic immune reactions against colon carcinoma cells, and only I-RNA's from the lymphocytes of breast cancer patients mediated immune reactions against breast cancer target cells. Allogeneic I-RNA extracted from peripheral blood lymphocytes of cancer patients possibly mediated specific cytotoxic immune reactions that were directed against common tumor-associated antigens shared by human tumors of similar histologic type.

Cholesterol and phospholipid biosynthesis in guinea pig megakaryocytes.

Megakaryocytes are the bone marrow cells which produce the blood platelets. Platelet lipids are thought to be important determinants of platelet activity in thrombosis and hemostasis. We have investigated lipid synthesis from [U-14C]-acetate in isolated guinea pig megakaryocytes with the goal of elucidating the genesis of platelet lipids. Cholesterol was the major product of megakaryocyte lipid synthesis from [U-14C]acetate. Incorporation of acetate (0.1 mM) into cholesterol per 10(6) megakaryocytes (1.1 mg protein) was 0.14 nmol in 0.5 h, 0.95 nmol in 1.5 h and 3.2 nmol in 4.0 h. Megakaryocytes also synthesized cholesterol from [U-14C]glucose. In contrast, platelet sterol synthesis was negligible. Both megakaryocytes and platelets synthesized phospholipids from [U-14C]acetate. Megakaryocytes incorporated 0.07 nmol acetate per 10(6) cells into phospholipid in 0.5 h, 0.38 nmol in 1.5 h and 1.8 nmol in 4.0 h. Platelets (10(9) cells, 1.3 mg protein) incorporated 0.15 nmol acetate into phospholipids in 1.5 h. Phosphatidylcholine accounted for 62% of the phospholipid radioactive label in megakaryocytes and 78% in platelets. Phospholipid radioactivity was associated with the fatty acids. We hypothesize that the megakaryocyte may synthesize a major portion of platelet cholesterol and that the phospholipid and fatty acid synthetic pathways available to the platelet are derived from the megakaryocytes.

Cholesterol exchange in platelets, erythrocytes and megakaryocytes.

Cholesterol exchange between plasma and human platelets and erythrocytes and guinea pig platelets, erythrocytes and megakaryocytes was studied. The characteristics of exchange of cholesterol between [3H]cholesterol-labeled plasma and human platelets and erythrocytes were similar: exchange per cell was independent of cell concentration in whole plasma, decreased only 2-fold over a wide range of cell concentrations in low concentrations of plasma and approached a plateau at 1/3 normal plasma cholesterol concentration, and there was no net change in the cholesterol content of either cell. The activation energy for exchange for both cells was 47 kJ/mol. In all experiments, erythrocyte cholesterol was labeled to approximately twice the specific activity of platelet cholesterol. Guinea pig megakaryocyte cholesterol exchanged at 25-33% of the rate of guinea pig platelet cholesterol in vitro. Similarly, when guinea pigs were fed [3H]cholesterol, erythrocyte cholesterol specific activity after 24 h was 90%, platelet 50-65%, and megakaryocyte 20-26% that of plasma. Guinea pig platelets incubated with plasma radiolabeled in free and esterified cholesterol incorporated radioactivity from free but not esterified cholesterol. The similarity of free cholesterol exchange in platelets and erythrocytes in vitro and in vivo and the apparent inability of platelets to take up cholesterol esters from lipoproteins suggest that the interaction between normal platelets and normocholesterolemic plasma is limited to cholesterol exchange.

The effect of hypercholesterolemia on guinea pig platelets, erythrocytes and megakaryocytes.

This study has examined the effect of diet-induced hypercholesterolemia on guinea pig platelets, erythrocytes, megakaryocytes and plasma. The cholesterol/phospholipid ratios of plasma and erythrocytes began to increase after one day on the diet and increased steadily for two weeks and more slowly thereafter until 30 days. In contrast, the cholesterol/phospholipid ratio of platelets remained constant for 4-5 days, then increased until reaching a maximum of about 0.85 in two weeks. Thus, the time-course for increase of the cholesterol/phospholipid ratio is different for platelets than for erythrocytes and plasma. The increase in the cholesterol/phospholipid ratio of megakaryocytes was small and not dependent on the degree of increase in the plasma cholesterol/phospholipid ratio. The cholesterol esters of both platelets and megakaryocytes increased with time for two weeks. The increase in megakaryocyte cholesterol esters appeared to precede that of platelets. The protein content of platelets and megakaryocytes and average megakaryocyte size were increased. Normal platelets incubated in plasma from hypercholesterolemic guinea pigs did not accumulate excess cholesterol, but erythrocyte cholesterol increased 45% in 6 h under the same conditions. Cholesterol synthesis in megakaryocytes was depressed 50-80% by cholesterol feeding and by in vitro incubation of the cells in hypercholesterolemic plasma. The data suggest that the platelets and erythrocytes may accumulate excess cholesterol by different mechanisms. The effects of cholesterol feeding on megakaryocytes and the lag in accumulation of cholesterol in platelets relative to erythrocytes and plasma suggest that a defect in the megakaryocyte may be a primary determinant of accumulation of cholesterol in platelets.

Effects of marine oil-enriched diets on guinea pig megakaryocyte and platelet lipids: effects on thromboxane synthesis and platelet function.

The effects of marine oil-enriched diets on the fatty acid composition of lipids in guinea pig megakaryocytes (MK) and platelets were studied to obtain a better understanding of the mechanisms for changes in platelet fatty acid composition and platelet function. Animals were fed 2%, 5% and 10% menhaden oil-enriched diets for up to 35 days. Platelets and MK were isolated and MK subpopulations at various stages of development were prepared. The diets did not cause a change in the cholesterol/phospholipid ratio in MK or platelets. The diets induced a dose related incorporation of eicosapentaenoic (20:5) and docosahexaenoic acid (22:6) and an associated decrease in linoleic acid (18:2) in both MK and platelets. However, there was a considerable greater depression of 20:4 in platelets than in MK. These changes were evident with 2% marine oil diets and maximal with 10% diets. Half maximal changes in fatty acid composition occurred after 3 days and maximal changes at 10 days after the initiation of the diets and no further changes occurred up to 35 days. Based on percent of total fatty acids in individual phospholipids, 20:5 had been primarily incorporated into phosphatidylethanolamine (PE) and phosphatidylinositol (PI) and 22:6 into PE and phosphatidylserine (PS) in both MK and platelets. 18:2 was decreased in all phospholipids. 20:4 was decreased only in PI in MK while 20:4 was decreased in PE, PI and PS in platelets. In animals on the 10% marine oil diet, more 20:5 and 22:6 were incorporated into mature than immature MK but the greatest amount of 20:5 and 22:6 had accumulated in platelets. Ingestion of marine oil-enriched diets did not cause thrombocytopenia or affect MK maturation based on the analysis of morphologic stage, ploidy or size. Marine oil-enriched diets caused a decrease in thromboxane synthesis in response to thrombin and calcium ionophore in platelets and MK at all stages of maturation. In platelet-rich plasma, collagen induced platelet aggregation, ATP secretion and thromboxane synthesis were decreased to a greater degree at 35 days than 10 days. Thus, the study indicates that the ingestion of marine oil-enriched diets resulted in the compartmentalization of 20:5 and 22:6 in acidic phospholipids in mature MK and platelets. The observation that marine oil-enriched diet induced maximal changes in lipid composition in MK and platelets within 10 days but caused progressive inhibition of platelet function for up to 35 days indicates that as yet undefined membrane and cellular changes may occur at later time points.

Arachidonate synthesis and uptake in isolated guinea-pig megakaryocytes and platelets.

Arachidonic acid (20:4) synthesis and uptake were studied in guinea-pig megakaryocytes and platelets. Isolated megakaryocytes and platelets were incubated with [3H]20:4, 8,11,14-[14C]eicosatrienoic acid (gamma-20:3) and [14C]linoleic acid (18:2) and their lipids were analyzed for radioactivity. The study showed that there was 0.153 microM of unesterified 20:3 and 0.237 microM of 20:4 in guinea-pig plasma in nonfasting animals. At these concentrations, 42.6 pmol of gamma-20:3 and 53.3 pmol of 20:4 were taken up per h per 10(5) megakaryocytes in vitro. Megakaryocytes desaturated 27% of the gamma-20:3 to 20:4 but could not desaturate 18:2. Platelets could not desaturate gamma-20:3 or 18:2. In megakaryocytes, the distribution of 20:4 synthesized by the desaturation of gamma-20:3 and 20:4 taken up reflected the endogenous distribution of 20:4 in megakaryocyte phospholipids and 20:4 was predominantly incorporated into phosphatidylethanolamine (PE). In contrast, the distribution of [3H]20:4 taken up into platelets did not reflect the endogenous distribution. 20:4 was primarily incorporated into platelet phosphatidylcholine and phosphatidylinositol. The study showed that megakaryocytes but not platelets possess a delta 5 desaturase and can synthesize 20:4 from gamma-20:3. Neither cell was shown to have a delta 6 desaturase. Megakaryocytes appear to have the capacity to determine the composition of all pools of platelet 20:4 either by uptake or synthesis of 20:4. Platelets, most likely, have a limited capacity to alter structural pools of 20:4 contained primarily in PE and phosphatidylserine (PS).

Lipid composition of guinea pig platelets and megakaryocytes. The megakaryocyte as a probable source of platelet lipids.

Platelets are formed by fragmentation of the cytoplasm and plasma membrane of the megakaryocyte in the bone marrow. This study has compared the lipid composition of guinea pig platelets and megakaryocytes. Phospholipids were quantitated by TLC and measurement of lipid phosphorus. Cholesterol and fatty acids were quantitated by GLC. The cholesterol/phospholipid molar distribution in megakaryocytes was: 9.8% phosphatidylserine, 6.7% phosphatidylinositol, 14.2% sphingomyelin, 40.0% phosphatidylcholine and 29.3% phosphatidylethanolamine. Platelets continued 11.2% phosphatidylserine, 5.1% phosphatidylinositol, 16.1% sphingomyelin, 38.6% phosphatidylcholine and 29.0% phosphatidylethanolamine. The major megakaryocyte fatty acids were 20.0% palmitic, 16.4% stearic, 20.6% oleic, 13.2% linoleic and 8.2% arachidonic. The major platelet fatty acids were 17.4% palmitic, 17.5% stearic, 11.6% oleic, 12.4% linoleic and 14.6% arachidonic. The major and minor fatty acid compositions of the individual platelet phospholipids reflected those of the megakaryocyte counterparts. The increased arachidonic acid and decreased oleic acid in platelets relative to megakaryocytes were found in all four glycerophospholipids. The similarity of the phospholipid and fatty acid composition of megakaryocytes and platelets suggests that the lipid composition of the platelet is determined by the megakaryocyte.

Distribution of phosphatidylethanolamine arachidonic acid in platelet membranes.

Arachidonic acid (20 : 4) and other fatty acids and aldehydes in phosphatidylethanolamine (PE) present on the platelet surface was determined. Surface-exposed PE was isolated by using 2,4,6-trinitrobenzenesulfonate, a non-penetrating probe (Schick, P.K., Kurica, K.B. and Chacko, G.K. (1976) J. Clin. Invest. 57, 1221--1226). PE contains 50% total platelet arachidonic acid. Approx. 16% platelet PE is present on the platelet surface. The study showed that the fatty acid and aldehyde composition of PE on the platelet surface is virtually identical to that in PE present inside the platelet. Therefore, 8 nmol arachidonic acid are present in PE in the outer layer of the plasma membrane in 10(9) platelets.

Lower motor neuron disease in a patient with autoantibodies against Gal(beta 1-3)GalNAc in gangliosides GM1 and GD1b: improvement following immunotherapy.

We followed a patient with a lower motor neuron form of motor neuron disease whose neurologic disorder improved following immunotherapy. The patient did not have an M protein but did have IgM antibodies to ganglioside GM1 detectable at serum titers of 1:2,000 by ELISA. These antibodies were found only in the IgM fraction with lambda light chains and immunoreacted with GD1b and Gal (beta 1-3) GalNAc.

Acute radiation injury of mice and the influence of sudden time shift.

The daily light-dark regimen for two groups of mice was advanced by 8 hr. A third group remained in unchanged lighting conditions. At seven different times within the following day subgroups of the time-shifted mice as well as of the group with unchanged time schedule were exposed to whole-body X irradiation. Mortality, body weight, and temperature of each animal were registered for 30 days following exposure and were regarded as indicators of radiation response. Radioresistance was found to be highest after two-thirds of the daily light span, confirming earlier reports by other authors. Well-defined effects of time shift and a corresponding shift of the maximum of radioresistance could be demonstrated. With the individual body weight as an independent variable, mathematical formulas for survival prognosis could be established.

Experimental chemotherapy of radiation injury with synthetic lysophospholipid analogs in mice.

Synthetic lysophospholipids represent a variety of analogs of the naturally occurring 2-lysophosphatidylcholine. Some of these compounds showed significant therapeutic effects on the survival of mice following radiation injury when administered after various doses of whole-body X irradiation. Such therapeutic effects were discernible even when the treatment was given 6 hr after irradiation, and both intravenous and oral application were effective. Intravenous application of 2 X 25 mg/kg lysophospholipid after whole-body X irradiation around the LD50 resulted in significantly higher numbers of surviving animals. The mode of action remains speculative.

Arterial catheter embolization followed by surgery for large chemodectoma.

We report on the first successful preoperative arterial catheter embolization of a large neck chemodectoma followed by its surgical removal. A 21-year-old man presented with a large mass in the right neck diagnosed 5 years previously by biopsy as a chemodectoma. The patient previously had refused therapy. Because of concern over the large size of the mass and increasing difficulty in swallowing, he agreed to undergo therapy. The patient underwent selective occlusion of the occipital and posterior auricular arteries and the thyrocervical trunk using Ivalon sponge emboli injected through a No. 5 Fr Hanafee catheter. A postembolization arteriogram showed 90% occlusion of tumor vascularity and 30% decrease in size of the tumor. This was followed by removal of the tumor surgically. A review of the difficult management of the patient is presented, and implications for future use of the combined procedures are discussed.

Contact plate thermography: a new technique for diagnosis of breast masses.

Ninety-four consecutive patients who underwent breast biopsy were prospectively evaluated with contact plate thermography. Final diagnosis based on surgically excised tissue was used as the standard of comparison. There were 77 benign lesions and 17 malignant lesions in the study group. A diagnosis of cancer was made by contact plate thermography in 11 of the 17 patients with malignant neoplasms, with six false-negative diagnoses. Among the 77 histologically benign lesions, contact plate thermography made the correct diagnosis in 66 cases, with 11 false-positive results. Considering all 94 patients, contact plate thermography was accurate in 81.9%, with 6.4% false-negative and 11.7% false-positive diagnoses. These data compared favorably with other diagnostic data used in this study, namely physical examination and mammography. Contact plate thermography is a quick, inexpensive, and harmless diagnostic procedure. Further evaluation of it is indicated, including its possible inclusion in breast cancer screening programs.

Immune responses in the treatment of advanced carcinoma of the breast. Effects of adrenalectomy.

We set out to answer the question, "Is the effect of adrenalectomy associated with or mediated through the immune response?" Eleven patients were studied preoperatively and postoperatively by in vitro immunologic tests. The assay system used included absolute T cell counts, phytohemagglutinin (PHA) blastogenesis, leukocyte adherence inhibition (LAI) after contact with 3M potassium chloride breast antigens, and blocking as measured in the blastogenesis and LAI assays. Good correlation was found between favorable clinical response to adrenalectomy and a rise in the number of absolute T cells, an increase in LAI positivity, and a decrease in blocking as measured by LAI blocking assay, but no correlation was seen in PHA blastogenesis assays. The association of clinical objective responses and improved immune responses is of significance.