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We consider a dynamical system with state space M, a smooth, compact subset of some R(n), and evolution given by T(t), x(t)=T(t)x, x in M; T(t) is invertible and the time t may be discrete, t in Z, T(t)=T(t), or continuous, t in R. Here we show that starting with a continuous positive initial probability density rho(x,0)>0, with respect to dx, the smooth volume measure induced on M by Lebesgue measure on R(n), the expectation value of logrho(x,t), with respect to any stationary (i.e., time invariant) measure nu(dx), is linear in t, nu(logrho(x,t))=nu(logrho(x,0))+Kt. K depends only on nu and vanishes when nu is absolutely continuous with respect to dx.(c) 1998 American Institute of Physics.

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The bioequivalence of two sustained-release preparations of quinidine bisulphate from Teva (Israel) and from Astra (Sweden) was assessed in an acute, single-dose randomized cross-over study in seven healthy subjects. There was no significant difference in time to peak, peak serum concentration, area under the concentration time curve from 0 to infinity, and the fraction absorbed between quinidine bisulphate 500 mg from Teva and from Astra. In addition, quinidine bisulphate 250 mg from Teva was compared with the short-acting quinidine sulphate 200 mg. The quinidine bisulphate from Teva had a significantly P less than 0.025) decreased peak serum concentration and an increased time to peak compared with the short-acting quinidine sulphate, although these two drugs are similar for the area under the curve from 0 to infinity. Our pharmaceutical records show that 85% of outpatients receiving quinidine are given the sustained-release quinidine bisulphate. However, only 36% of the outpatients prescribed sustained-release quinidine bisulphate are appropriately prescribed for twice-daily treatment. Thus the quinidine bisulphate from Teva is a sustained-release preparation with bioequivalence to the reference sustained-release preparation and can be administered twice daily.

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We determined the state of the leukocyte adhesiveness/aggregation in the peripheral blood by using a simple slide test and found it to be more sensitive than the white blood cell count for the detection of acute mental stress. Included were 71 controls, 64 young athletes examined just before their exercise, 14 volunteers who were examined 10-20 min before engagement in rappelling while an additional group of 20 were examined just before the act as they were facing an abyss from the top of a cliff. The state of leukocyte adhesiveness/aggregation correlated significantly (p less than 0.0005) only with the increasing strain assumed to occur from the first to the fourth group. The state of leukocyte adhesiveness/aggregation was 3.3 x more sensitive than white blood cell count in both rappelling groups and 5 x more sensitive than white blood cell count when evaluated in those examined at the last minute. We concluded that the state of leukocyte adhesiveness/aggregation is a reliable marker of acute mental stress.

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Investigation of patients with suspected or proven hypoglycemia is often a time-consuming and expensive process. We describe a glucose reduction challenge test which may be useful as an out-patient screening procedure. Insulin is infused for 3 h at 40 mU/kg.h. Plasma glucose was monitored at the bedside during the test, and blood samples were collected for measurement of C-peptide. Responses were examined in 17 normal controls, and 6 patients with insulinomas. In normal subjects, mean plasma glucose fell to a plateau value of 3.2 +/- 0.2 mmol/L (57 +/- 2.6 mg/dL) and remained at that level with few symptoms. In contrast, five of six patients with insulinomas developed severe hypoglycemia, with plasma glucose levels between 1.9 (34 mg/dL) and 2.2 mmol/L (39 mg/dL). Plasma C-peptide concentrations were suppressed to 0.08 pmol/mL or less in normal subjects, but in insulinoma patients remained at 0.32-1.6 pmol/mL i.e. outside the normal range, and diagnostic of nonsuppressible insulin secretion. These data demonstrate that moderate reduction of serum glucose maintained for a prolonged period results in marked suppression of plasma C-peptide, permitting improved discrimination between normal subjects and patients with insulinomas. This glucose reduction challenge can, therefore, be used as a test of glucose-regulating ability, where failure (hypoglycemia) per se represents a measurable abnormality. C-Peptide measurements will determine whether the cause of hypoglycemia is due to hyperinsulinemia.

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Catheter blockage in patients receiving long-term parenteral nutrition with fat-containing total nutrient admixture (TNA) is a relatively common complication. A study was carried out to characterize the material which is filtered out of the TNA and is a potential cause of catheter blockage. A total of 45 bags containing the same TNA solution were stored for 7 days at 4 degrees C. The stability of the solution in all the bags was then confirmed by light microscope and Coulter Counter, to determine the particle-size distribution, following which the solution was filtered through a 5-microns filter. Chemical analysis was then made to determine the amount of solid particles, fat and precipitates of Mg, Zn, Ca, Na, and K in the filter contents. Each bag was found to contain 7326 +/- 2681 solid particles as plasticizers and the main component of the filter contents was fat (99.4%) whereas electrolytes as precipitates constituted less than 0.5%. The amount of fat and electrolytes lost on the filter from the solution was negligible. Our analysis of the material trapped on the filter, which may block the catheter during long-term therapy, suggests the importance of filtration and of finding a means for dissolving the fat, the main component of the filter material.

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Somatostatin has been widely used to suppress endogenous pancreatic hormone secretion in research studies. Many of these studies required the simultaneous infusion of a hormone together with somatostatin. A critical assumption for its use in metabolic investigation is that somatostatin has no effect on the action or clearance of a concomitantly infused hormone. To test whether clearance of an exogenously infused hormone is affected, we infused insulin with or without somatostatin in two sets of studies. Insulin (40 mU X kg-1 X h-1) was infused for 100 min (n = 6). Plasma glucose levels fell to 55 +/- 4.1 mg/dl with insulin alone and significantly lower, to 44 +/- 1.9 mg/dl, when somatostatin (250 micrograms/h) was also infused (P less than .01). Plasma immunoreactive insulin (IRI) rose to 57 +/- 12.5 microU/ml with insulin alone, which was significantly different from 88 +/- 15 microU/ml when insulin was infused together with somatostatin (P less than .01). When a smaller dose of insulin (30 mU X kg-1 X h-1) was infused for 100 min (n = 4), similar results were observed. When somatostatin was infused together with insulin, plasma glucose fell to lower levels (41 +/- 4.2 vs. 62 +/- 9.5 mg/dl; P less than .01) and plasma IRI rose higher (39 +/- 8.5 vs. 27 +/- 5.9 microU/ml; P less than .01) than when insulin was infused alone. C-peptide was equally suppressed by hypoglycemia regardless of whether somatostatin was administered, indicating suppression of endogenous insulin during these studies. We conclude that somatostatin infusion impairs the clearance of exogenous insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

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The purpose of this study was to detect the possibility of drug interference in the estimation of urine protein in patients receiving therapeutic doses of penicillin G, ampicillin, methicillin, cefoxitin, cefazolin, gentamicin, co-trimoxazole, phenothiazines, glibenclamide and acetazolamide. Five different methods for urine protein determination were compared in these patients, when different amounts of albumin were added to urine in vitro, and in a control group of patients not treated with drugs known to interfere with these methods. The techniques included two semi-quantitative tests--a strip test (Albustix) and heat and acetic acid turbidity test; and three quantitative tests--sulphosalicylic acid test, trichloroacetic acid test and a test based on a formation of Ponceau S dye-protein complex (Urin-Pak). The only significant interference found was that of gentamicin with the Ponceau S dye test.

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The route and schedule of treatment with high-molecular levan markedly influences its inhibitory effect on the growth of transplanted AKR lymphoma. Injections of levan into the site of the primary tumor were more effective in inhibiting tumor growth and preventing tumor-associated weight loss and mortality than were i.p. injections. Local levan injections inhibited metastatic spread only in mice treated from Days 0 and 2. Levan i.p. was more effective in inhibiting metastases in animals started on treatment 7 to 13 days after tumor inoculation than in animals in which levanization was started earlier. Local injection of levan before inoculation of tumor enhanced tumor growth and shortened life-span in comparison to nonlevanized animals. In mice treated with levan for a short period only, the inhibitory effect on tumor growth slowly vanished within 2 weeks. Some animals treated for 5 to 8 months remained completely free of tumor. The results indicate that the effect of levan on tumor development is mainly topical and depends on the concentration of the polysaccharide in the site. The tumor growth period from 0 to 5 days appears to differ from the following period in the reaction to levan treatment. The nature of this difference is not clear, but possible explanations are discussed.

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Levan was shown to inhibit lymphoma development in AKR mice. Growth of tumor was inhibited at the site of injection and in metastases. Levan caused a decrease in the incidence of tumors, and it reduced pleomorphism, mitoses, and invasiveness of tumors in comparison to nonlevanized mice. Evidence of tumor cell destruction was observed in levanized mice. The effect of levan on tumor development was dose dependent.

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The effect of oral administration of brewer's yeast on resistance to infectious diseases was studied in laboratory animals. It was shown that there was a significantly increased enhancement of resistance to seasonal respiratory and enteric infections in rhesus monkeys. Similarly, enhanced resistance to experimental chronic infections was observed in mice after yeast administration. A 2-week lag occurred between the initiation of yeast treatment and the expression of enhanced resistance. Study of the mechanism of the yeast-induced enhancement of resistance to infection leads to the conclusion that it is based on in vivo stimulation of phagocytosis, as measured by the "phagocytic index." No effect of brewer's yeast on circulating antibody levels was detected.

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