Characterization of hyperinsulinemic recombinant inbred (RI) strains (SMXA-5 and SMXA-9) derived from normoinsulinemic SM/J and A/J mice.

We discovered two mouse strains (SMXA-5 and SMXA-9) with hyperinsulinemia among the substrains and progenitor strains (SM/J and A/J) of the SMXA recombinant inbred (RI) strains, and characterized the two strains at 20 weeks of age. SMXA-5 (mean +/- S.E.M: 9.6 +/- 1.7 ng/ml) and SMXA-9 (7.7 +/- 1.3 ng/ml) males had higher serum immunoreactive insulin levels than SM/J (1.4 +/- 0.3 ng/ml) and A/J (1.1 +/- 0.1 ng/ml) males in the nonfasting condition. The hypoglycemic response to insulin at 30 min after injection was significantly less in SMXA-5 males than in SM/J mice. Glucose tolerance test revealed that the incidence of impaired glucose tolerant males was 58% (11/19) in SMXA-5 and 42% (10/24) in SMXA-9 strains, but none in SM/J and A/J strains. SMXA-5 (209 +/- 29 mg/dl) and SMXA-9 (235 +/- 31 mg/dl) had higher serum triglyceride levels than SM/J (126 +/- 14 mg/dl) and A/J (89 +/- 5 mg/dl) males in the nonfasting condition. Histologic examination revealed enlarged islets in the pancreas of hyperinsulinemic SMXA-5 male mice. Moreover, SMXA-5 and SMXA-9 mice exhibited mild obesity. SMXA-5 and SMXA-9 males were therefore characterized by hyperinsulinemia, impaired glucose tolerance, hypertriglyceridemia and mild obesity which resembled some of the phenotypes of human Syndrome X, although both progenitor strains were normal so far as we examined. Since the RI strains are a powerful tool to facilitate polygenic-trait analysis, SMXA-5 and SMXA-9 mice will be useful materials to investigate the genetic basis of complex diseases, and are possible new metabolic models in relation to hyperinsulinemia.     

Alpha-1-antitrypsin: frequencies of PiM subtypes and serum concentration in the Japanese population

PiM subtypes were determined by isoelectric focusing of the sera of 746 Japanese at the age of 16-60 years. The gene frequencies were calculated: PiM1 = 0.7855, PiM2 = 0.1528 and PiM3 = 0.0617. The serum concentration of alpha-1-antitrypsin was measured by laser-nephelometric immunoassay of the sera of 284 individuals. A statistically significant difference (p less than 0.01) in the serum concentration was found between M1 (2.63 +/- 0.67 g/l) and M1M2 (2.39 +/- 0.59 g/l).     

The serum protein content of human follicular fluid and its correlation with the maturity of oocytes

The authors determined, by an immunochemical method, the alpha-1-antitrypsin, Gc globulin, prealbumin, albumin, haemopexin, transferrin, haptoglobin, IgA, IgG, ceruloplasmin, alpha-2-macroglobulin contents of 98 follicular fluids, 10 peritoneal fluids and 24 blood sera. Out of these proteins analysed, change in the concentration of alpha-1-antitrypsin showed correlation with the maturity and fertilisation of the oocyte. The alpha-1-antitrypsin content was 1.6 +/- 0.26 g/l in the case of mature oocytes, and 3.1 +/- 1.12 g/l in the case of immature ones. Fertilisation was also concomitant of low alpha-1-antitrypsin levels.     

Growth of Allescheria boydii in anitbiotic-containing media

Cazin, John, Jr. (University of Iowa, Iowa City), and David W. Decker. Growth of Allescheria boydii in antibiotic-containing media. J. Bacteriol. 90:1308-1313. 1965.-Thirteen isolates of Allescheria boydii were surveyed for their ability to grow and sporulate on media containing cycloheximide and chloramphenicol. The fungus grew well in the presence of 4 to 8 mg/ml of cycloheximide, whereas ascocarps and coremia were always inhibited at a concentration of the drug lower than that required to inhibit growth and conidial production. In certain strains, ascocarp production was inhibited by concentrations of cycloheximide (0.4 mg/ml) normally used in selective media; however, two strains produced mature ascocarps at a concentration of 1 mg/ml of the antibiotic, and two strains produced immature ascocarps at a concentration of 4 mg/ml. Growth inhibition was not observed with concentrations of chloramphenicol as high as 1,000 mg per liter in any of eight strains tested.     

Effect of estrogens on renal responsiveness to parathyroid hormone in elderly female subjects

The effect of estrogens on the renal responsiveness to parathyroid hormone (PTH) was examined by PTH loading tests with synthetic human-PTH (1-34) in 8 normal elderly females (mean +/- SD age, 81.0 +/- 7.1 yr) before and after administration of estrogen (Premarin 1.25 mg/day for 4 weeks). Basal urinary adenosine cyclic 3', 5'-monophosphate (cAMP) excretion showed a tendency to increase after estrogen administration (5.47 +/- 1.68 vs 6.60 +/- 2.67 nmol/100 ml GFR) and the theoretical renal phosphorous threshold showed a tendency to decrease from 3.22 +/- 0.98 to 2.73 +/- 0.56 mg/dl. The blood ionized calcium concentration did not change after estrogen administration (4.44 +/- 0.16 vs 4.32 +/- 0.20 mg/dl) and serum phosphorous (P) decreased significantly (3.65 +/- 0.47 vs 3.01 +/- 0.42 mg/dl, p less than 0.05). There was no increase in mean serum immunoreactive PTH (0.34 +/- 0.10 vs 0.34 +/- 0.05 ngeq/ml). The urinary excretions of cAMP in response to PTH loading [100 U of human-PTH (1-34), intravenously] significantly (p less than 0.05) increased (94.8 +/- 57.0 vs 196.7 +/- 118.3 nmol/100 ml GFR/h) after estrogen administration. Moreover the changes in urinary excretion of cAMP (r = 0.698, p less than 0.01) and P (r = 0.555, p less than 0.05) induced by the PTH loading were positively correlated with serum estradiol in elderly females, assessed as groups before and after estrogen administration. These results suggest that estrogens may enhance the renal responsiveness to exogenous PTH administration.     

Comparison of the carbohydrate and amino acid composition of normal and S-variant alpha-1-antitrypsin.

alpha-1-Antitrypsin has been isolated and purified from the serum of an individual with the Pi S phenotype whose serum contains only 50--60% as much alpha-1-antitrypsin as normal M-type serum. The preparation was homogeneous by the criteria of sodium dodecyl sulfate polyacrylamide gel electrophoresis and sedimentation equilibrium ultracentrigufation. When analyzed in the ultracentrifuge, the S-type alpha-1-antitrypsin exhibited a molecular weight of 47,500 which was essentially the same as that of the M-type (47,300) and the Z-type (47,500) alpha-1-antitrypsin. The S-type alpha-1-antitrypsin contains 15.2% carbohydrate consisting of 16.4 residues/mol of N-acetylglucosamine, 7.8 residues/mol of mannose. 6.7 residues/mol of galactose and 7.1 residues/mol of sialic acid which is essentially the same as the carbohydrate composition of the M-type alpha-1-antitrypsin. In addition, M- and S-type alpha-1-antitrypsin have very similar amino acid compositions.     

Isolation and characterization of alpha-1-antitrypsin from rhesus-monkey serum.

A simple, relatively gentle, procedure for isolation of rhesus-monkey alpha-1-antitrypsis from serum is described. The method consists of chromatographic separation of the fraction precipitated by 50-75%-satd. (NH4)2SO4 from pooled monkey serum on DEAE-cellulose followed by affinity chromatography on Sepharose-bound concanavalin A. Approx. 30% of the trypsin-inhibitory activity present in the original serum was recovered when alpha-1-antitrypsin was reconstituted with physiological saline (0.85% NaCl). Pure alpha-1-antitrypsin exhibitied a single band on sodium docecyl sulphate/polyacrylamide-gel electrophoresis, with an estimated mol.wt. of 60000 and four bands in acid/starch-gel electrophoresis. The acid/starch-gel-electrophoretic pattern and mobility of isolated material were identical with those of the alpha-1-antitrypsin bands in the original serum sample. The most rapdily migrating bands resembled the pattern and mobility for the normal human phenotype PiM in 28 monkeys. A starch strip from the acid/starch-gel-electrophoresis as the origin for antigen-antibody electrophoresis was used to examine alpha-1-antitrypsin for microheterogeneity; no evidence for microheterogeneity was observed in samples from 18 monkeys. In addition, isolated alpha-1-antitrypsin exhibited a single arc when subjected to immunoelectrophoresis. Amino acid and carbohydrate compositions of isolated monkey alpha-1-antitrypsin were similar to those of human alpha-1-antitrypsin.     

Acute phase response of plasma proteins in analbuminemic rats

In healthy Nagase analbuminemic rats (NAR), the highest degree of relative increase in serum protein concentration was found for alpha-2-macroglobulin, the most prominent acute phase protein in rats. Its levels were about 30- and 60-fold higher in males and females, respectively, than those in the control Sprague-Dawley (SD) rats. In terms of absolute concentration, however, alpha-1-inhibitor 3 (also called alpha-X-protein or murinoglobulin) showed the most conspicuous change, its levels being higher by about 7 mg/ml than those in SD. When the acute phase reaction was induced by subcutaneous injection of turpentine, the levels of alpha-1- and alpha-2-macroglobulins, alpha-1-cysteine proteinase inhibitor, alpha-1-antiproteinase, and alpha-1-inhibitor 3 in NAR changed in essentially the same way as in SD: alpha-1-inhibitor 3 decreased markedly while the rest increased further. These results suggest that mechanisms responsible for the elevation of serum globulins in healthy NAR are not directly related to those involved in the acute phase response. On the other hand, the antithrombin III levels in healthy NAR were about twice the control values and changed little during the inflammation. In contrast, this protein in SD doubled during the acute phase, its maximal levels being close to those in healthy or inflamed NAR. This suggests that the antithrombin III level in healthy NAR is regulated by a mechanism similar to that in SD maximally reacting to the acute phase stress.(ABSTRACT TRUNCATED AT 250 WORDS)     

Immunological profiles in workers occupationally exposed to inorganic mercury.

Forty-one male mercury-exposed workers were examined for the serum concentration levels of immunoglobulins (IgG, IgA, IgM), alpha-1-antitrypsin (A1AT), alpha-2-macroglobulin (A2M), ceruloplasmin (CPL) and orosomucoid (ORO). In the period preceding this investigation the mercury concentrations in workplace air ranged from 0.106 to 0.783 mg.m-3, the range of urinary mercury concentrations was from 0.029 to 0.545 mg.1(-1). All but two (IgG and A1AT) of the immune parameters tested were at the levels that were evidently higher than those found in a control group of 55 workers matched by age who lived in a relatively clean area. The percentage of individuals with no value out of the range of normal physiological limits was in the controls almost 80%, in the exposed 36.6% only. These findings confirm the literature data which show that an inhalation exposure to inorganic mercury may evidently have a stimulating effect on some serum proteins in humans.     

Activity of selected proteinase inhibitors in patients with disorders of lipid metabolism]

The study was aimed at verification of previously found, in animals with experimentally induced atherosclerosis, the disturbances of serum proteinases inhibitors: alpha-2-antiplasmin, alpha-1-antitrypsin and alpha-2-macroglobulin. In humans with hypercholesterolemia the decrease of serum activity of alpha-2-antiplasmin was observed. In humans with hypercholesterolemia and increased serum concentration of triacylglycerols no significant changes in activity of alpha-1-antitrypsin and alpha-2-macroglobulin were found--in comparison with control subjects.     

A Pro → Leu substitution in codon 369 of the alpha-1-antitrypsin deficiency variant PI MHeerlen

Summary The molecular defect has been elucidated in the alpha-1-antitrypsin (PI) gene of a patient with a serum level of only 5 mg/100 ml and a PI M-like phenotype, designated PI MHeerlen. The restriction fragment patterns obtained by probes covering the whole gene and flanking sequences were normal, suggesting no major rearrangements. The nucleotide sequence of the exons, intron/exon junctions, and a part of the promoter region is similar to that of a PI M1(Ala²¹³) gene except for an CT mutation in codon 369, causing a ProLeu substitution. Haplotype analysis and oligonucleotide hybridization studies demonstrated the homozygous state of the mutation in the index case. It is most likely that the Pro³⁶⁹Leu substitution is responsible for the low serum alpha-1-antitrypsin concentration of the patient because this mutation is solely confined to the PI MHeerlen allele and no other relevant mutations could be revealed. As proline is important for the secondary and tertiary structure of proteins, the mutation may cause an abnormal processing of the nascent polypeptide. The same mutation was observed in two unrelated subjects known to carry a PI allele giving a low serum alpha-1-antitrypsin level.     

Separation and quantitation of serum beta-carotene and other carotenoids by high performance liquid chromatography

We describe a specific assay for serum provitamin A (alpha- and beta-carotene) by high pressure liquid chromatography (HPLC). The system separates alpha- and beta-carotene in 7.4 min using a C18 muBondapak, 10-micron particle size column with a mobile phase of acetonitrile-chloroform 92:8 at 2 ml per min and a 462 nm detector. The HPLC assay had a recovery of 94.8% of added beta-carotene and, at a serum concentration of 215.2 micrograms/L, had within-run and between-run precisions of 3.1% and 3.6%, respectively. In 65 subjects, the HPLC-determined provitamin A (alpha- and beta-carotene) value was 343 +/- 166 micrograms/L and averaged 23.4 +/- 7.9% (range 9-43%) of the values obtained by a traditional colorimetric assay for total serum "carotenes." Although total serum carotenes showed no relationship to serum vitamin A (r = -0.048; P = 0.78), HPLC-determined alpha- and beta-carotene was significantly inversely correlated (r = -0.357; P = 0.05).     

Radioimmunoassay of melatonin: human serum and cerebrospinal fluid

Using a newly characterized anti-melatonin serum it has been possible to establish human serum melatonin concentrations at short time intervals during 24h. A clear circadian rhythm with peak values during the dark phase was demonstrated in both men and women. Values (pg/ml;mean +/- SE) were as follows: females 02.00h: 130 +/- 7, 18.00h: 45 +/- 5 males 02.00h: 140 +/- 11, 18,00H: 70 +/- 5. The estimation (pg/ml; mean +/- SE) of melatonin in human serum (males: 63 +/- 22 and females: 100 +/- 45) and cerebrospinal fluid simultaneously taken has shown that melatonin is lower in cerebrospinal fluid (males: 59 +/- 33 and females: 57 +/- 28). Blanks are not subtracted.     

Whole blood and serum copper levels in relation to sex and age

The copper content in whole blood and serum was determined in healthy human subjects (240 males and 217 females) by atomic absorption spectrophotometry. The mean level of copper obtained in whole blood was 104.8 +/- 20.5 micrograms/100 ml in males and 117.1 +/- 20.1 micrograms/100 ml in females. The mean level of copper in serum was 102.3 +/- 21.7 micrograms/100 ml and 123.9 +/- 30.4 micrograms/100 ml, in males and females respectively. The copper concentration in whole blood and serum in females proved to be significantly higher than in males (p less than 0.001). With respect to age, the copper level showed a slightly negative correlation which is only statistically significant in whole blood in females (p less than 0.05).     

Alpha-2 and beta-adrenergic receptors mediate NE's biphasic effects on rat thick ascending limb chloride flux

The sympathetic neurotransmitter norepinephrine (NE) influences renal sodium excretion via activation of adrenergic receptors. The thick ascending limb (THAL) possesses both alpha-2 and beta-adrenergic receptors. However, the role(s) different adrenergic receptors play in how isolated THALs respond to NE are unclear. We tested the hypothesis that both alpha-2 and beta-adrenergic receptors are responsive to NE in the isolated THAL, with alpha-2 receptors inhibiting and beta-receptors stimulating chloride flux (J(Cl)). THALs from male Sprague-Dawley rats were perfused in vitro, and the effects of 1) incremental NE, 2) the alpha-2 agonist clonidine, and 3) the beta-agonist isoproterenol on J(Cl) were measured. Low concentrations (0.1 nM) of NE decreased J(Cl) from a rate of 114.2 +/- 8.1 to 93.5 +/- 14.6 pmol. mm(-1). min(-1) (P < 0.05), with the nadir occurring at 1 nM (67.7 +/- 8.8 pmol. mm(-1). min(-1); P < 0.05). In contrast, greater concentrations of NE significantly increased J(Cl) from the nadir to a maximal rate of 131.0 +/- 28.5 pmol. mm(-1). min(-1) at 10 microM (P < 0.05). To evaluate the adrenergic receptors mediating these responses, the THAL J(Cl) response to NE was measured in the presence of selective antagonists of beta- and alpha-2 receptors. A concentration of NE (1 microM), which alone tended to increase J(Cl), decreased THAL J(Cl) (from 148.9 +/- 16.4 to 76.2 +/- 13.6 pmol. mm(-1). min(-1); P < 0.01) in the presence of the beta-antagonist propranolol. In contrast, a concentration of NE (0.1 microM), which alone tended to decrease J(Cl), increased THAL J(Cl) (from 85.5 +/- 20.1 to 111.8 +/- 20.1 pmol. mm(-1). min(-1); P < 0.05) in the presence of the alpha-2 antagonist rauwolscine. To further clarify the role of different adrenergic receptors, selective adrenergic agonists were used. The alpha-2 agonist clonidine decreased J(Cl) from 102.4 +/- 9.9 to 54.0 +/- 15.7 pmol. mm(-1). min(-1), a reduction of 49.1 +/- 11.0% (P < 0.02). In contrast, the beta-agonist isoproterenol stimulated J(Cl) from 95.3 +/- 11.6 to 144.1 +/- 15.0 pmol. mm(-1). min(-1), an increase of 56 +/- 14% (P < 0.01). We conclude that 1) the sympathetic neurotransmitter NE exerts concentration-dependent effects on J(Cl) in the isolated rat THAL, 2) selective alpha-2 receptor activation inhibits THAL J(Cl), and 3) selective beta-receptor activation stimulates THAL J(Cl). These data indicate the response elicited by the isolated rat THAL to NE is dependent on the neurotransmitter concentration, such that application of NE in vitro biphasically modulates J(Cl) via differential activation of alpha-2 and beta-adrenergic receptors in a concentration-dependent manner.     

Radioimmunoassay of 5-androstene-3 beta,17 beta-diol in plasma and in breast cyst fluid

A simple and reliable radioimmunoassay for the determination of 5-androstene-3 beta, 17 beta-diol in peripheral plasma and in breast cyst fluid, after a chromatography on Celite microcolumn has been described and evaluated. The antiserum used was raised in rabbits injected with dehydroepiandrosterone-15 alpha-(O-carboxymethyl)-bovine serum albumin. In men below 40 years of age the levels ranged from 0.85 to 2.80 ng/ml (mean +/- SEM: 1.52 +/- 0.11; n = 24) and from 0.50 to 2.20 ng/ml (mean +/- SEM: 0.93 +/- 0.09; n = 20) in men aged between 41 and 62 years. The mean level was significantly different (P less than 0.001) between the 2 groups. A significant correlation (r = -0.56; P less than 0.01) was demonstrated between age and all male levels. In females the mean plasma level was in the follicular phase: 0.81 +/- 0.07 ng/ml (range: 0.40-1.50; n = 17; age: 19-41 years) and in the luteal phase: 0.83 +/- 0.05 ng/ml (range: 0.40-1.30; n = 29; age: 18-43 years). No cyclical change and no correlation with age could be evidenced. A significant difference (P less than 0.001) was shown between females and the young male group. In breast cyst fluid the levels ranged from 0.05 to 13.70 ng/ml (mean +/- SEM: 2.36 +/- 0.86; n = 20) whereas the sulfate concentrations ranged from 75 to 7500 ng/ml (mean +/- SEM: 1891 +/- 565; n = 15), thus demonstrating very wide inter-individual variations.     

Cytidine-5'-monophosphate-N-acetylneuraminic acid. Asialoglycoprotein sialic acid transferase activity in liver and serum of patients with juvenile hepatic cirrhosis and alpha-1-antitrypsin deficiency.

The molecular basis for the accumulation of a substance which displays the immunological reactivity of alpha-1-antitrypsin within vesicles of liver parenchymal cells of individuals with hepatic cirrhosis and serum alpha-1-antitrypsin deficiency remains unclear. We recently reported that serum from a patient with alpha-1-antitrypsin deficiency and hepatic cirrhosis was substantially deficient in sialyltransferease (EC 2.4.99.1) an enzyme which transfers sialic acid from cytidine 5'-monophosphate-N-acetylneuraminic acid to a variety of asialoglycoprotein acceptors. In the present report we have extended these studies to include serum from five additional patients with alpha-1-antitrypsin deficiency and juvenile hepatic cirrhosis as well as a liver specimen obtained at autopsy of one of these patients. We find the sialytransferase activity in serum from six patients with alpha-1-antitrypsin deficiency and hepatic cirrhosis to be 50% of healthy pediatric control values and 30% of pediatric patients with liver disease. However, serum from family members homozygous for alpha-1-antitrypsin deficiency but without hepatic cirrhosis, and serum from patients with a variety of other kinds of liver disease, failed to exhibit the marked sialytransferase deficiency. Similar assays carried out on a homogenate of a liver sample from one patient with alpha-1-antitrypsin deficiency and hepatic cirrhosis indicated that the deficiency of sialyltransferase activity was not demonstrable in liver. Furthermore, a comparative kinetic analysis of serum and liver sialytransferase in normal and afflicted individuals failed to detect differences in substrate affinities which might account for a decrease in functional sialyltransferase capacity in individuals with alpha-1-antitrypsin deficiency and hepatic cirrhosis. These observations suggest that the serum sialyltransferase deficiency in such patients probably arises after chronic and extensive liver disease involving hepatic accumulation of alpha-1-antitrypsin rather than the enzyme deficiency being the primary cause of the hepatic cirrhosis and alpha-1-antitrypsin deficiency.     

Kinetics of improved extracellular beta-d-fructofuranosidase fructohydrolase production by a derepressed Saccharomyces cerevisiae

AIMS: beta-d-fructofuranosidase fructohydrolase (FFH, EC 3.2.1.26) is an enzyme which hydrolyses the alpha-1,4 glycosidic bonds of sucrose and releases monosaccharides. The present study deals with the kinetics of improved extracellular FFH production by Saccharomyces cerevisiae in batch culture. MATERIALS AND RESULTS: Strains of S. cerevisiae can show increased FFH activity when grown on chemically defined medium. In the present study, wild-culture S. cerevisiae GCB-IV was mutated by treatment with ethyl methane sulfonate (EMS). Among six yeast mutants, EMS-II was found to be the highest FFH-producing strain (51.46 +/- 2.4 U ml(-1)). Maximum FFH production (78.46 +/- 3.2 U ml(-1)) was obtained 48 h after incubation by this 2-deoxy-d-glucose (2dg)-resistant mutant (76.20 mg ml(-1) protein). The optimal concentration of sucrose, incubation period and initial pH were 30.0 g l(-1), 28 degrees C and 6.5, respectively. The mutant EMS-II showed improvement in FFH production when 5.0 g l(-1) urea was added as a sole nitrogen source into SAPY medium. Values for Q(p) (1.802 +/- 0.2 U ml(-1) h(-1)) and Y(p/s) (3.460 +/- 1.1 U g(-1)) of EMS-II were significantly improved over the other yeast strains. CONCLUSION: The E(a) value (40.28 +/- 3.5 kJ mol(-1)) of EMS-II was significant (P 相似文献   

Dehydroepiandrosterone therapy in men with angiographically verified coronary heart disease: the effects on plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA) and fibrinogen plasma concentrations

INTRODUCTION: The aim of this study was to analyze the influence of DHEA therapy on fibrinogen, plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) plasma concentrations in men with decreased serum DHEA-S levels and angiographically verified coronary heart disease (CHD). MATERIAL AND METHODS: The study included thirty men aged 41-60 years (mean age 52 +/- 0.90 yr) with serum DHEA-S concentration < 2000 mg/l, who were randomized into a double-blind, placebo-controlled, cross-over trial. Subjects completed the 80 days study of 40 days of 150 mg oral DHEA daily or placebo, and next groups were changed after 30 days of wash-out. Fasting early morning blood samples were obtained at baseline and after each treatment to determine serum hormones levels (testosterone, DHEA-S, LH, FSH and estradiol) and also fibrinogen, plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) plasma concentrations. RESULTS: Administration of DHEA was associated with 4.5-fold increase in DHEA-S levels. Estrogen levels significantly increased after DHEA from 22.1 +/- 0.7 pg/ml to 26.4 +/- 1.6 pg/l (mean +/- SEM; p < 0.05), while testosterone levels did not changed. Fibrinogen concentrations significantly decreased in DHEA group from 4.5 +/- 0.3 g/l to 3.83 +/- 0.2 g/l (p < 0.05 vs. placebo). Changes of tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) were not statistical significant (respectively: 8.37 +/- 0.4 ng/ml vs. 8.93 +/- 0.5 ng/ml and 82.3 +/- 6.3 ng/ml vs. 92.7 +/- 9.1 ng/ml (mean +/- SEM; NS vs. placebo). Tolerance of the treatment was good and no adverse effects were observed. CONCLUSIONS: DHEA therapy in dose of 150 mg daily during 40 days in men with DHEAS levels < 2000 mg/l and angiographically verified coronary heart disease (CHD) was connected with significant decreasing of fibrinogen concentration and increasing of estradiol levels, and did not influence on plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) plasma concentrations.     

消炎痛对四氧嘧啶引起的大鼠糖尿病的保护作用

本工作观察了预先给予消炎痛对四氧嘧啶引起的糖尿病大鼠血糖、血清胰岛素和胰高血糖素浓度的影响。结果表明:预先皮下注射消炎痛能使糖尿病大鼠血糖浓度明显降低,并且具有明显的量效关系。在消炎痛剂量5,10,15mg/kg时,注射四氧嘧啶48h后血糖浓度由对照组的591.5±38.2mg％分别降低到559.1±53.2,463.2±16.6和266.6±29.9mg％。在注射消炎痛10mg/kg的实验组,血清胰岛素浓度由对照组的10.5±2.7μU/ml增加到31.9±7.0μU/ml,胰高血糖素由对照组的550.0±27.0pg/ml降低到303.1±22.9pg/ml。组织学观察结果表明,消炎痛对四氧嘧啶引起的大鼠胰岛β细胞的损伤具有显著的保护作用。