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N Kern

Publications and source records attributed to N Kern.

8 recordsLinked to original sources
PubMed2004

Two-dimensional viscous froth model for foam dynamics.

The two-dimensional viscous froth model is a simple tractable model for foam rheology and coarsening. It includes, but is not confined to, the quasistatic regime. Here we present a detailed analysis and implementation of the model, illustrated with various examples. With certain simplifying assumptions, it provides significant insight into strain-rate-dependent effects in foam rheology and elsewhere, particularly in relation to recent experiments.

Journal Article↗
PubMed2003

Pharmacological and nonpharmacological factors influencing hypothalamic-pituitary-adrenocortical axis reactivity in acutely depressed psychiatric in-patients, measured by the Dex-CRH test.

The most consistent biological findings in patients with depression are abnormalities in the hypothalamic-pituitary-adrenal (HPA)-axis, which can be measured using the combined dexamethasone-suppression/CRH-stimulation (Dex-CRH) test. The reactivity of the HPA-axis in this test, however, ranges over several orders of magnitude in depressed patients with comparable severity of symptoms. In this present study, we investigate which factors influence the magnitude of the response in the Dex-CRH test in 235 acutely depressed in-patients. We first examined the effects of common confounders shown to influence the HPA-axis, such as caffeine and nicotine consumption, acute stressors during the test, weight, gender, and age. Of all these variables, only female sex and nicotine consumption were positively correlated with the cortisol or ACTH response, respectively. As for the effects of psychopharmacological treatment, only the intake of carbamazepine and the fact of having relapsed under an established pharmacotherapy significantly increased the response in the Dex-CRH test, whereas the presence or absence of antidepressant treatment, the type of antidepressant treatment, or the number of ineffective antidepressant treatment trials during the index episode up to admission did not have any effect. We also found a positive correlation of the number of previous episodes, the overall HAM-D score and the severity of somatic/vegetative symptoms with the results in the Dex-CRH test. These results underline that in depressed patients this test is not majorly influenced by disease-unrelated factors. In addition, current antidepressant treatment does not appear to affect test outcome in the absence of clinical response. The influence of the number of previous episodes and relapse under pharmacotherapy suggests that HPA-axis reactivity may be altered by repetitive states of hypercortisolemia or continuous antidepressant treatment. Finally, more severe vegetative symptoms are associated with an enhanced HPA-axis activity.

Adrenocorticotropic Hormone↗
PubMed2001

Paraoxon sensitive phenylvalerate hydrolase in assessing the severity of acute paraoxon poisoning.

INTRODUCTION: Intoxications with organophosphorous compounds, especially paraoxon, are frequent. Organophosphorous compounds inhibit serine hydrolases such as acetylcholine, butyrilcholine, and carboxyl esterases although acetylcholine and butyrylcholine are too sensitive to paraoxon to be useful markers of severity. They cannot show a dose-dependent inhibition during an acute organophosphorous compounds exposure because maximal enzyme inhibition is reached at very low organophosphorous compounds concentrations. PURPOSE: To determine in vitro the dose-effect relationship between the activity of the paraoxon-sensitive phenylvalerate hydrolase, a member of the carboxvl esterases family, and the paraoxon dose, and to assess its utility as a putatively less sensitive enzyme marker to monitor the severity of an acute paraoxon intoxication. MATERIALS AND METHODS: Phenylvalerate hydrolase and butyrylcholine activities were determined in serum of nine healthy human volunteers before and after addition of different concentrations of paraoxon. The determination of phenyl-valerate hydrolase activity was carried out using a modification of the method described by Johnson. A commercially available kit was used to measure butyrylcholine activity. RESULTS: Paraoxon inhibits phenyl-valerate hydrolase activity at concentrations above 10 M. Maximal inhibition (approximately 50% of baseline) is achieved at concentrations above 2.5 x 10(-7) M. The IC50 value of paraoxon for phenyl-valerate hydrolase is 34+/-2 nM. The uninhibited phenyl-valerate hydrolase activity is due to paraoxon-resistent isoforms. Paraoxon begins inhibiting butyrylcholine activity at concentrations above 10(-9) M. At concentrations above 5 x 10(-5) M, no butyrylcholine activity is measulrable. The IC50 value of paraoxon for butyrylcholine is 150+/-23 nM. CONCLUSION: The paraoxon-sensitive subunit of phenyl-valerate hydrolase shows dose-dependent inhibition when exposed to paraoxon in vitro, but it is even more sensitive than butyrylcholine to paraoxon inhibition. Determinations of phenyl-valerate hydrolase activity to assess the severity of an acute organophosphorous compounds poisoning cannot be recommended, but phenyl-valerate hydrolase may have utility in worker surveillance.

Biomarkers↗
PubMed1991

Diagnosis of sleep-disordered breathing by half-night polysomnography.

We hypothesized that sleep-disordered breathing (SDB), defined by the apnea index (AI), the apnea + hypopnea index (A + H/I), or the desaturation event frequency (number of desaturations greater than 5%/h slept) (DEF), could be diagnosed after less than full-night polysomnography (PSG). Forty-eight consecutive full-night PSG sessions were evaluated by separately analyzing the first half (PSG-1/2) and the total (PSG-T) sleep time: 134.42 +/- 35.7 and 277.15 +/- 56.5 min (mean +/- SD), respectively. PSG-1/2 and PSG-T were not different with respect to AI. The DEF was statistically but not clinically higher during PSG-1/2 (41.72 +/- 41 versus 37.95 +/- 35.8, p = 0.04). Sensitivities, specificities, and predictive values of each PSG-1/2 parameter were determined by comparing the values with those measured during PSG-T, using cutoff frequencies of both 5 and 10 events/h slept to define SDB. At a cutoff frequency of 10, sensitivities and positive predictive values were high for all PSG-1/2 parameters (range, 94.6 to 96.9%). The specificities of the DEF and AI during PSG-1/2 were also high (93.75 and 95%, respectively), but the negative predictive value of the DEF was substantially better (93.75 versus 83.3%). With SDB defined by 5 events/h slept, there also were high sensitivities (87.9 to 93%), positive predictive values (93.6 to 100%), and specificities (86.7 to 100%) for all parameters. Negative predictive values, however, were substantially reduced (62.5 to 76.5%). We conclude that PSG during 2 h of sleep is an appropriate method for evaluating SDB.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation Studies as Topic↗
PubMed1990

Obstructive sleep apnea treated by independently adjusted inspiratory and expiratory positive airway pressures via nasal mask. Physiologic and clinical implications.

Treatment of obstructive sleep apnea with nasal continuous positive airway pressure mandates simultaneous increases of both inspiratory and expiratory positive airway pressures to eliminate apneas as well as nonapneic oxyhemoglobin desaturation events. We hypothesized that the forces acting to collapse the upper airway during inspiration and expiration are of different magnitudes and that obstructive sleep-disordered breathing events (including apneas, hypopneas and nonapneic desaturation events) could be eliminated at lower levels of EPAP than IPAP. To test these hypotheses, a device was built that allows the independent adjustment of EPAP and IPAP (nasal BiPAP). Our data support the hypotheses that expiratory phase events are important in the pathogenesis of OSA and that there are differences in the magnitudes of the forces destabilizing the upper airway during inspiration and expiration. Finally, applying these concepts, we have shown that by using a device that permits independent adjustment of EPAP and IPAP, obstructive sleep-disordered breathing can be eliminated at lower levels of expiratory airway pressure compared with conventional nasal CPAP therapy. This may reduce the adverse effects associated with nasal CPAP therapy and improve long-term therapeutic compliance.

Algorithms↗
PubMedDate not supplied

L-lactate reduces in vitro the inhibition of butyrylcholinesterase (BChE) by paraoxon (E 600).

Intoxication with the organophosphorus compound paraoxon (POX), an inhibitor of serine hydrolases, is frequent. Oximes are the only enzyme reactivators clinically available. Serendipitous observation led us to the hypothesis that lactate might attenuate some of the POX effects. In vitro effects of lactate on the inhibition of butyrylcholinesterase (BChE) by POX were assessed in plasma of 12 healthy human volunteers. The determinations were repeated using different lactate and different POX concentrations. The BChE activity determinations were performed in the following settings: (i) baseline untreated plasma (BL); (ii) after addition of POX to plasma (pl+POX); (iii) after POX and plasma were incubated and then lactate was added (pl+POX/lact); (iv) after addition of lactate to plasma (pl+lact); (v) after lactate and plasma were incubated and then POX was added (pl+lact/POX); (vi) after lactate and POX were incubated and then added to plasma (lact+POX/pl). In the micro- and millimolar ranges, lactate is able to abolish in vitro the inhibition of BChE by POX in human plasma when added to plasma prior to POX or when incubated with POX prior to addition to plasma. Lactate added to plasma after POX has no protective effect. In a second set of experiments, the effect of lactate on BChE activity was determined. At high millimolar concentrations, lactate itself inhibits BChE to an extent comparable to POX. Lactate is a mixed inhibitor of BChE, being able to interfere with the enzyme-substrate complex (inhibition constant for the enzyme-inhibitor-substrate complex K'I(EIS) = 81 mM) and the enzyme (inhibition constant for the enzyme-inhibitor complex K(I) (EI) = 26 mM).

Butyrylcholinesterase↗