Search PubMed⌕ Search

Biomedical subjects

J Nowak

Publications and source records attributed to J Nowak.

At least 127 records · Page 7Linked to original sources
PubMed1988

Auxin induced stress tolerance in algae.

IAA effect on responses of West African algae Caloglosa, Bostrychia, Rhizoclonium and the fresh water alga Pithophora to different growth conditions was examined in growth chamber experiments. The auxin (2.28 x 10(-5) M) caused growth increase of 2.3- and 2.6-fold in Caloglossa and 1.6 and 1.7 in Rhizoclonium, respectively, in sea water and 1:1 diluted sea water/Erdschreiber medium. In Bostrychia pronounced deterioration of growth was noticed in the control samples between 16 and 32 days in culture. The cultures maintained an active growth, however, in the presence of IAA. IAA also allowed Pithophora to withstand salinity: Compared to growth in fresh water, a 65% growth inhibition was recorded in 1:1 diluted sea water in the absence of auxin and a slight growth stimulation when the auxin was present. Pithophora and Rhizoclonium also maintained higher rates of growth in extremal temperatures of 10 and 45 degrees C when the auxin was present.

Journal Article↗
PubMed1988

The yeast aminopeptidase Y.

A metal-dependent aminopeptidase (EC 3.4.11.-), designated APase Y, has been purified to homogeneity by conventional methods. The enzyme is composed of a single polypeptide chain with molecular mass of 102 kilodaltons, estimated by sodium dodecyl sulphate - polyacrylamide gel electrophoresis, with a blocked N-terminal amino acid. It possesses neither endopeptidase nor carboxypeptidase activity and is strongly inhibited by metal-chelating agents, Zn2+, and the protein inhibitor from Neurospora crassa. APase Y is insensitive to Cl anions, S--S reducing reagents, serine protease inhibitors, and the peptidase inhibitor benzamidine. Co2+, Hg2+, and p-chloromercuribenzoate can activate the enzyme up to 22, 20, and 55%, respectively. The holoenzyme is resistant to yeast endopeptidases A, B, and Y, whereas the apoenzyme (obtained after treatment with chelators) is susceptible to the serine endopeptidases B and Y. The enzyme catalyzes hydrolysis of most L peptides possessing free alpha-amino (or imino) group by stepwise removal of N-terminal residue. Peptides with L-leucine at the N terminus are cleaved preferentially. The enzyme is unable to catalyze hydrolysis of X--Pro type peptide bonds, and inefficiently hydrolyzes bonds between Asp--X and Glu--X. L-leucine p-nitroanilide hydrolyzes optimally at pH 8.2 with a Km value of 1 mM. The purified enzyme is stable during storage in 0.05 M phosphate buffer, pH 6.7, containing 40-50% glycerol, at -20 degrees C.

Amino Acid Sequence↗
PubMed1987

Vascular effects of infused adenosine are not mediated by prostacyclin release in humans.

Adenosine may contribute to the regulation of tissue blood flow directly and via release of vasoactive substances. For example, in the isolated, perfused heart, the nucleoside has been reported to release prostacyclin, a potent vasodilator. In humans, minor variations in prostacyclin release into the circulation result in readily detectable changes in the urinary excretion of its metabolite, 2,3-dinor-6-ketoprostaglandin (PG) F1 alpha, as measured by negative ion-chemical ionization gas chromatography-mass spectrometry. To test the hypothesis that prostacyclin participates in or mediates the vascular effects of adenosine, we administered adenosine (5.1 mg/min) or vehicle to healthy volunteers in random order as a 2-h infusion into the femoral artery under double-blind conditions. The plasma levels of adenosine, inosine, and hypoxanthine increased significantly during infusion of active drug, but the urinary excretion of adenosine and uric acid were unchanged, implying efficient tissue uptake of the infused nucleoside. Adenosine, but not vehicle, significantly (P less than 0.01) increased leg blood flow (from 2.7 +/- 0.3 to 8.7 +/- 2.5 ml X 100 ml tissue-1 X min-1), heart rate (from 66 +/- 3 to 80 +/- 4 beats/min), and urinary epinephrine excretion (from 2.8 +/- 0.4 to 5.4 +/- 0.8 ng/mg creatinine). In contrast, the excretion of 2,3-dinor-6-keto-PGF1 alpha was unaltered by infusion of adenosine. We confirmed that biologically significant alterations in prostacyclin release in the lower limb vascular bed would be reflected by the urinary metabolite in experiments involving local infusion of prostacyclin at a rate below the threshold necessary to alter limb blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Biochemical evidence of a chronic abnormality in platelet and vascular function in healthy individuals who smoke cigarettes.

Cigarette smoking is associated with increased mortality from cardiovascular disease that declines after cessation. This study extends the evidence regarding the effects of chronic smoking on platelets and the vessel wall in vivo. Excretion of a major urinary thromboxane metabolite, 2,3-dinor-thromboxane B2, is significantly (p less than .01) elevated in apparently healthy chronic smokers (20 cigarettes daily) compared with that in nonsmoking control subjects. This difference in excretion of 2,3-dinor-thromboxane B2 was abolished by the administration of 20 mg aspirin twice daily, a dose shown to selectively inhibit platelet cyclooxygenase. After aspirin, the return of the excretion of 2,3-dinor-thromboxane B2 to pretreatment levels paralleled the recovery of platelet cyclooxygenase. These findings indicate that excessive thromboxane A2 generation in chronic smokers predominantly derives from platelets. The urinary excretion of the prostacyclin metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha also is increased during chronic cigarette smoking, as is the case with other diseases associated with accelerated interaction of platelets with the vessel wall. We have found evidence of platelet and vascular dysfunction in vivo in chronic cigarette smokers before the manifestation of overt cardiovascular disease. The results would also be consistent with the hypothesis that in chronic smokers, the platelet defect is largely reflective of smoking-induced vascular injury.

Adult↗
PubMed1986

Measurement of renal and non-renal eicosanoid synthesis.

Enzymatic metabolites of arachidonic acid (eicosanoids) have potent biologic actions in vitro that suggest their pathophysiologic importance in vivo. To address this possibility, analytic methodology has been developed to permit study of the formation of these compounds in vivo. Both radioimmunoassay and gas chromatography-mass spectrometry have been used to measure stable but biologically inactive metabolites of the eicosanoids. Although indirect, such measures are presently the most reliable, because superfusion-bioassay lacks the specificity and precision necessary for quantitative analysis of eicosanoid formation in vivo. Measurement of eicosanoids and their hydration products and metabolites in urine represents a non-invasive approach to the assessment of eicosanoid biosynthesis. Although a tissue of origin cannot be ascribed definitely to a compound measured in urine, corroborative evidence can be obtained to indicate the predominant tissue source under physiologic and pathologic conditions. This relates particularly to the distinction between renal and extrarenal biosynthesis of these compounds. Although similar limitations apply to the measurement of eicosanoids in plasma, these may also be confounded by sources of artifact related to blood withdrawal. In the case of thromboxane B2, these concerns have been addressed by the development of methods to measure its enzymatic metabolites in plasma. Finally, formation of eicosanoids may be studied in localized compartments such as lavage or synovial fluid. Such an approach has recently provided biochemical evidence for increased formation of prostacyclin and prostaglandin E2 at the platelet-vascular interface during selective inhibition of thromboxane synthase in humans.

Arachidonic Acid↗
PubMed1986

Effect of nicotine on prostacyclin formation in human endocardium in vitro.

The effect of nicotine on the formation of prostacyclin by human endocardium was studied in vitro. Slices of cardiac valve cusps were incubated in a saline medium and the prostacyclin-like activity generated spontaneously by the tissue specimens was assessed in terms of its capacity to inhibit ex vivo platelet aggregation. In separate experiments supernatants of valvular tissue homogenates were incubated with [14C]arachidonate. This resulted in the appearance of labelled 6-keto-prostaglandin F1 alpha in the radiochromatograms, indicating the formation of prostacyclin in the homogenates. Nicotine inhibited dose-dependently the spontaneous generation of prostacyclin-like activity (I50 approximately equal to 2 X 10(-4) M), as well as the formation of 6-keto-prostaglandin F1 alpha (I50 approximately equal to 2 X 10(-5) M), indicating an inhibitory effect of the drug on endocardial prostacyclin production.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

[Insulin secretion and utilization of insulin in piglets after insulin, arginine and glucose loads].

The insulin secretion and utilization dynamics have been investigated in 35 six weeks old healthy piglets in order to find the connection with spontaneous hypoglycemia. The trial to load piglets with insulin showed an average time t1/2 = 4.93 minutes accepted as normal in 10 piglets with the mean increase in body weight equal to 0.19 kg/day, prolonged time t1/2 = 7.56 minutes in 7 piglets with the decreased gain of body weight to 0.108 kg/day, and short time t1/2 = 2.78 minutes with the poor gain of body weight in 6 piglets at the age of 6 weeks. In 10 weeks old piglets the noted time t1/2 was 14.7 minutes. The trial to load piglets with L-arginine--HC1 showed a high insulin secretion amounting to 105.5 microU/ml of plasma in 3 piglets only, assumed as correct, and a low insulin secretion amounting to an average of 20.5 microU/ml of plasma in 10 piglets corresponding, according to the criteria of diagnostics, to the subclinical form of human diabetes mellitus. The glucose tolerance test enabled to distinguish 7 strongly reacting piglets (over 100 microU/ml of plasma), 10 moderately responding piglets (from 20 to 100 microU/ml), and 2 piglets not responding (16 microU/ml) by means of increase in insulin concentration. The differentiated results with the individuals deviations to subclinical values observed in healthy piglets, point to serious difficulties in the maintenance of the equilibrium between insulin secretion and utilization. Excessive secretion lasting over 2 hrs and very fast utilization of insulin as well as the level of glucose not compensated by gluconeogenesis, can be the cause of hypoglycemia.

Animals↗
PubMed1986

Thyroid hormones and insulin in milk; a comparative study.

Thyroid hormones (TH) in milk can be measured by RIA after prolonged extraction with alkaline ethanol at low temperature. The results of this method agreed with those obtained by gas chromatography-mass spectrometry, though they show the concentrations lower than in most of the already published studies based on radioimmunoassay. The levels of thyroxine (T4) in colostrum and milk in rabbit, cow and women were found to be similar, about 2 nmol l-1, which represented a small fraction of those in blood serum. Triiodothyronine (T3) content approximated one third of that in serum and was about 1.0, 1.8, 0.3 and 0.5 nmol l-1 in the rabbit, pig, human and cow, respectively. Although in a relatively high blood concentration, reverse-T3 does not appear in cow milk, but it passes through the blood/mammary gland barrier into the milk in rabbits in which it appears in a very low concentration. Of TH in milk, T3 may exert some physiological role in offsprings, particularly during the early adaptive postnatal period. Insulin (INS) in human, cow and pig milk was found in concentrations approximate to those in blood serum. They were high at the peri-parturient period and then fell rapidly in the pig and more gradually in the women, to a relatively low and constant levels. Transfer of INS into the mammary gland and milk was positively related to the actual concentrations of this hormone in the blood, in quantities which, following ingestion of milk, might exert some biological action in neonates.

Animals↗
PubMed1985

Is hyperventilation a physiologically significant stimulus for prostaglandin release in the human pulmonary vascular bed?

The influence of hyperventilation on the pulmonary prostaglandin (PG) release was studied in healthy volunteers. Hyperventilation was forced by adding 8% CO2 to the inhaled air and arterial and mixed venous blood was sampled for radioimmunoassays of 6-keto-PGF1 alpha and PGE2. The increased ventilation did not alter the arterio-venous PG concentration differences suggesting that hyperventilation accompanying the activation of chemoreceptors is not a physiologically significant stimulus for the pulmonary PG release in man.

6-Ketoprostaglandin F1 alpha↗