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Biomedical subjects

M Bauer

Publications and source records attributed to M Bauer.

At least 325 records · Page 18Linked to original sources

Adverse events and tolerability of the combination of fluoxetine/lithium compared with fluoxetine.

Data from an intensive observational drug utilization study were analyzed to determine whether patients who received the combination of fluoxetine and lithium had more and different adverse events as compared with those receiving fluoxetine alone. In a matched cohort control design, we compared 110 patients per group. Results showed no significant difference in side effects between groups. Also, the incidence of "serotonergic" adverse events showed no significant differences between groups during the 7-week study period. In conclusion, the results show that the combination of fluoxetine/lithium is generally well tolerated in spite of a somewhat increased rate of minor side effects.

Adult↗

Neurological syndromes in factitious disorder.

Factitious disorder is characterized by the intentional feigning of physical or psychological signs and symptoms. The best known type of factitious disorder, Munchausen syndrome, is marked by a chronic unremitting course with repeated hospitalizations. The purpose of this study was to assess the frequency, psychopathological phenomenology, and diagnostic classification according to DSM-III-R in patients with factitious disorder presenting as neurological syndromes. We prospectively included all patients who were hospitalized at our Department of Neurology, Freie Universität Berlin, during a 1-year period. Five of 1538 (.3%) patients were diagnosed as having factitious disorder with feigning of neurological syndromes. Four presented with the classic variant, Munchausen syndrome. All patients had similar, characteristic psychopathological features including self-discharge, aggressive behavior, pseudologia phantastica, and hospital wandering. In these cases the additional diagnosis of personality disorder was made according to DSM-III-R criteria. We concluded that factitious disorder presenting with neurological syndromes may be more prevalent than generally assumed. Our findings confirm the idea of frequent coincidence of factitious and personality disorders.

Adult↗

Influence of pentoxifylline and albifylline on liver microcirculation and leukocyte adhesion after hemorrhagic shock in the rat.

The aim of this study was to evaluate the effects of two xanthine derivates, pentoxifylline (PTX) and its more metabolically stable analogue, albifylline (HWA 138), on hepatic sinusoidal perfusion and leukocyte endothelial interactions in the liver after hemorrhagic shock. Sprague-Dawley rats (n = 8 per group) were exposed to hemorrhagic shock at 40 mm Hg for 60 minutes and subsequently resuscitated with 60% of shed blood and lactated Ringer's solution before intravital microscopy of the liver 3 hours after resuscitation. Using fluorescence markers, quantitative evaluations of red blood cell (RBC) and white blood cell (WBC) velocities and WBC endothelium interactions were performed. Animals were chosen randomly and blindly to receive either PTX or HWA 138 in a dosage of 25 mg/kg body weight 1 minute before resuscitation, or they received placebo. This was followed by a further infusion of 25 mg/kg body weight during the 3-hour resuscitation period. Although systemic parameters were comparable in all groups, both xanthine derivates enhanced the reduced velocity of RBCs and WBCs of the placebo group. Pathological values of WBC endothelium adhesion in the placebo group (adhesion index: 126.7 +/- 19.5 s/100 WBCs, mean +/- SE) was significantly reduced by PTX (64.4 +/- 10.5, p < 0.05) and HWA 138 (71.9 +/- 10.7, p < 0.05). The results indicate a significant reduction of shock-induced leukocyte adhesions to the sinusoidal endothelium in the liver. In addition, both xanthine derivates led to improved microvascular blood flow in the liver. Thus, PTX and HWA 138 reveal multiple positive effects on early shock-induced alterations in the liver, supporting earlier studies which indicated their potential application in shock therapy.

Animals↗

High energy phosphates and direct calorimetry as predictive parameters for metabolic recovery of the rat liver following ischemia.

BACKGROUND AND METHODS: Alteration of the hepatocellular function following ischemic damage may play a crucial role in the limited recovery after reperfusion. In spite of numerous efforts, finding a simple technique for predicting recovery of the liver after ischemic damage is still an unresolved problem. During ischemic storage of isolated rat livers at 25 degrees C tissue concentrations of high energy phosphates and lactate were determined photometrically and interstitial pH was measured by glass electrodes. In comparison, the metabolic rate was measured continuously by direct calorimetry. In a second series of experiments these results were compared with functional recovery after ischemia and reperfusion. Following ischemic storage at 25 degrees C for 60, 120 or 240 min, the isolated livers were reperfused for 30 min in a non-recirculating system with a constant flow rate. During reperfusion functional recovery, as assessed by oxygen consumption and bile flow, was determined. At the end of reperfusion tissue samples were taken for biochemical analysis of adenine nucleotides. Furthermore, morphologic integrity was determined by electron microscopy. RESULTS: Whereas the ATP concentration drops within 60 min of ischemia to 6.9% of the control value without further significant change, the continuously measured metabolic rate as assessed by direct calorimetry decreases in an exponential manner. Accordingly, a better correlation of hepatocellular secretory function and calorimetrically measured heat output (r2 = 0.85; P < 0.001) was observed than with high energy phosphates (r2 = 0.56; P < 0.001). CONCLUSIONS: These data suggest that if the metabolism of the ischemic rat liver falls below a critical level, recovery is incomplete or impossible. Therefore, assessment of the global metabolic rate by direct calorimetry seems not only to be a very good predictor of recovery after ischemic damage but also a good tool in the laboratory for studies concerning the sequelae of ischemic metabolism and for improvement of tissue protection.

Adenine Nucleotides↗

Long-term observation of the hypothalamic-pituitary-thyroid (HPT) axis in alcohol-dependent patients.

Thyroid hormone levels and thyrotrophin (TSH) were measured in 45 alcohol-dependent patients before detoxification and 8 days, 3 months and 6 months after detoxification, and compared to levels in healthy controls. Before detoxification, levels of thyroxine (T4) and thyroxine-binding globulin (TBG) were significantly reduced in patients compared with healthy controls, while triiodothyronine (T3), reverse T3, and TSH levels did not differ from those in healthy controls. During the entire observation period, free T4 (fT4) and free T3 (fT3) levels were slightly elevated compared with those in healthy controls. T4 and TBG levels increased significantly during the first week of abstinence. Severity of withdrawal symptoms was negatively correlated with the total T4 levels after 8 days of abstinence. Three months after detoxification, relapsers displayed significantly lower T4 and TBG levels compared with abstinent patients. The increase in T3 levels was most pronounced between 8 days and 3 months of abstinence in both relapsing and abstinent patients. Six months after detoxification, only abstinent patients could be assessed, and they displayed increased TBG and T3 levels compared to healthy controls. Our findings suggest a different time-course for T3 and T4 levels after detoxification in alcohol-dependent patients, and indicate that T4 levels after detoxification interact with withdrawal symptoms.

Adult↗

Effect of fluconazole on fungicidal activity of flucytosine in murine cryptococcal meningitis.

Both animal and in vitro studies have demonstrated that combinations of flucytosine with amphotericin B and with fluconazole have significantly improved activity against cryptococcal meningitis compared with the activity of each drug used alone. However, very few dose levels of these agents have been tested in combination. This study evaluated the efficacy of fluconazole plus flucytosine in a murine model of cryptococcal meningitis over a broad range of dose combinations (fluconazole, 0 to 40 micrograms/g of body weight per day; flucytosine, 0 to 200 micrograms/g/day). Both drugs were dissolved in drinking water, with treatment on days 2 to 11. In this highly reproducible model, fluconazole had a dramatic effect on the fungicidal activity of flucytosine. Flucytosine at dose levels of as much as 200 micrograms/g/day alone or in combination with low doses of fluconazole had minimal fungicidal activity, whereas in combination with fluconazole at 24 to 40 micrograms/g/day, flucytosine showed fungicidal activity in the range of 45 to 65% of the animals treated at doses of 40 to 100 micrograms/g/day. This striking effect of fluconazole is consistent with the results of both in vitro and clinical studies. In the clinic, the use of flucytosine is often limited by severe toxicity, while toxicity is rarely observed with fluconazole. These results suggest that when flucytosine is given with higher doses of fluconazole, the maximum therapeutic effect of the former in the clinic may be observed at dose levels that are far less than the doses commonly employed (150 micrograms/g daily).

Animals↗

Evidence for a functional link between stress response and vascular control in hepatic portal circulation.

Heme oxygenase (HO)-derived carbon monoxide (CO) may contribute to vascular control through elevation of guanosine 3',5'-cyclic monophosphate. In the present study, we investigated the functional significance of expression of the isoenzyme HO-1 (heat-shock protein 32) in liver after hemorrhage/resuscitation (H/R) in rats anesthetized with pentobarbital sodium. An increase of mRNA levels for HO-1 was observed at 3 h after resuscitation, followed by induction of the protein at 6 h in pericentral hepatocytes and sinusoidal lining cells. Concomitantly, lower portal resistance was observed in H/R (0.33 +/- 0.060 mmHg.ml-1.min) compared with control rats (0.47 +/- 0.035 mmHg.ml-1.min). Blockade of the HO-CO pathway by tin protoporphyrin-IX (SnPP-IX) led to a transient increase in portal pressure with no effect on portal low in controls, whereas an increase in pressure and a decrease in flow contributed to the sustained increase in portal resistance after H/R. These results indicate that HO contributes to maintenance of hepatic perfusion in vivo under stressful conditions, suggesting a functional link between stress response and vascular control in portal circulation.

Animals↗

Endotoxin pretreatment enhances portal venous contractile response to endothelin-1.

To test whether endotoxin pretreatment modulates the portal hemodynamic response to endothelin (ET)-1 and phenylephrine (PE), two potent vasoconstrictors in the portal circulation of the normal liver, rats received intraperitoneal injections of Escherichia coli lipopolysaccharide (LPS; 1 mg/kg body wt) or saline. Livers were isolated after 6 or 24 h and perfused with Krebs buffer containing 5% autologous erythrocytes. Analyses of portal pressure-flow (P-Q) relationships and epifluorescence video microscopy were performed before and after ET-1 (10(-9) M) or PE (10(-5) M) administration. LPS pretreatment increased total portal resistances (Rt), zero-flow pressures (PQ = 0), and linear regression slopes of P-Q relationships, and decreased the sinusoidal diameters (Ds) and sinusoidal volumetric flow (Qv). The response to ET-1 was enhanced 6 and 24 h after LPS administration, leading to greater increases in Rt, PQ = 0, and slope and more pronounced decreases in Dx, red blood cell velocity (VRBC), and Qv. In contrast, PE effects were similar (PQ = 0, slope, Ds) or even attenuated (Rt, VRBC, Qv) in livers from LPS-treated compared with control animals. Thus endotoxin pretreatment increased the portal contractile response to ET-1 but not to PE. This enhanced ET-1 response appeared to occur at sinusoidal and presinusoidal levels and may contribute to endotoxin-induced hepatic microcirculatory failure.

Animals↗

A time-dependent balance between endothelins and nitric oxide regulating portal resistance after endotoxin.

To test whether endothelins are involved in the regulation of portal resistance after endotoxin pretreatment and whether their effects are modulated by nitric oxide (NO), rats received intraperitoneal injections of Escherichia coli lipopolysaccharide (LPS, 1 mg/kg body wt) or saline. Six and twenty-four hours later, livers were isolated and perfused. Analyses of portal pressure-flow (P-Q) relationships and epifluorescence microscopy were performed before and after administration of 1) the NO synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 10(-3) M), followed by L-arginine (2 x 10(-3) M), or 2) the endothelin ETA/ETB-receptor antagonist bosentan (2 x 10(-4) M), followed by L-NAME (10(-3) M). LPS pretreatment increased all measures of resistance, which included total portal resistance, zero flow, incremental resistance (slopes of P-Q relationship), and sinusoid resistance. L-NAME had no effect in sham controls but increased all measures of resistance at 6 h after LPS and increased total and incremental resistance 24 h after LPS. L-Arginine reversed these changes. Bosentan reduced total and sinusoid resistance slightly in control livers and caused substantial reductions in all measures of resistance at 6 and 24 h after LPS; these were partially reversed after L-NAME at 6 but not at 24 h. Our data support the hypothesis that a critical balance between endothelin-mediated vasoconstrictor influences and NO-mediated vasodilator influences controls portal resistance after endotoxin pretreatment.

Animals↗

Variability in the human entorhinal region may confound neuropsychiatric diagnoses.

The human entorhinal region consists of a number of areas; however, there is no generally accepted nomenclature for these cytoarchitectonic fields, and the designation of its constituent layers or strata is a matter of controversy. Here, we consider a hitherto neglected adjacent field, the preamygdaloid claustrocortex. Its medial subfield has a small common border with the rostromedial entorhinal region (width maximal 2 mm). Both fields are cytoarchitectonically rather similar. The rostromedial oral entorhinal field lacks ascending terminal islands. Its unusually small pre-alpha cells are arranged in a thin band or small clusters consisting of pyramidal, triangular, or polymorphic cells. The conspicuous chromophilic pre-beta cell clusters are composed of a variety of cell types, including groups of 'immature' spindle-shaped or bipolar nerve cells. Furthermore, a rare sulcus within the entorhinal region (central sulcus of the entorhinal region: observed in 4% of the 450 brains examined) is associated with an unusual lamination of the entorhinal layers in its wall and floor. Both the specific shape and arrangement of neurones in the claustrocortical-rostral entorhinal border region and the unusual lamination within the rare central entorhinal sulcus are regarded as reflecting neurodevelopmental disturbances characteristic of schizophrenic brains. In contrast, our observations in a large sample of serially sectioned brains from controls, schizophrenics, and patients suffering from neuropsychiatric diseases other than schizophrenia do not support this assumption.

Adult↗

Pulsatile and diurnal secretion of GH and IGF-I in the chronically catheterized pig fetus.

The ontogeny of GH and IGF-I secretion was investigated in the fetal pig. Pulse studies were performed to describe the pattern of GH release. Twenty-four-hour profiles were recorded to examine possible diurnal variations in these hormones. (I) PULSE STUDIES: Blood samples were obtained at 15-min intervals for 2-h periods from 24 male and 20 female fetuses at various gestational ages (fetal day 89-113; term 113 +/- 1 S.D.). Fetuses revealed a pulsatile GH release. The GH pulse frequency did not vary with gestational age in either sex (0.95 +/- 0.19 pulses/h). In males the GH pulse amplitude decreased with increasing fetal age (r = -0.41; P < 0.02). In female fetuses no significant correlation could be calculated. Mean GH concentrations fell significantly in male fetuses 3 to 4 days before delivery (P < 0.05) and the same tendency was observed in females (P < 0.06). Between fetal days 94 and 98 GH pulse amplitude and GH and IGF-I concentrations were higher in males than in females (P < 0.01, P < 0.001 and P < 0.02 respectively). Fetal IGF-I secretion showed no ontogenetic changes in both sexes. However, maternal IGF-I concentrations increased with progressing gestation (r = 0.46; P < 0.001). (II) 24-H PROFILES: Eight male and four female late-gestational fetuses (fetal days 104-108) were studied. Blood samples were taken at 30-min intervals over 24 h. Dams and fetuses showed an episodic GH secretion over the 24-h period but no diurnal rhythm was observed. Whereas maternal IGF-I secretion was constant, fetal IGF-I release was characterized by marked fluctuations over the 24 h. In half of the fetuses (n = 6) the fluctuations appeared at regular intervals. Again no diurnal rhythm existed. These data demonstrated that: (1) porcine fetal GH secretion is pulsatile and decreases shortly before birth; (2) a sex difference in GH and IGF-I concentrations exists between fetal days 94 and 98, suggesting that IGF-I is at least partially under the control of GH before birth; (3) fetal GH and IGF-I secretion is episodic over 24 h, but does not vary diurnally; and (4) fetal and maternal GH and IGF-I secretion are regulated independently.

Animals↗

Studies on the chronic oral toxicity of an analgesic drug combination consisting of acetylsalicylic acid, paracetamol and caffeine in rats including an electron microscopical evaluation of kidneys.

The analgesic drug combination Thomapyrin consisting of acetylsalicylic acid (CAS 50-78-2, ASA), paracetamol (CAS 103-90-2, NAPAP) and caffeine (CAS 58-08-2) in the ratio 5:4:1 was investigated for its chronic toxicity in rats. For comparison the individual drugs ASA and NAPAP as well as the double combination ASA+NAPAP were tested in equipotent doses. 20 male and 20 female rats per group (Chbb:THOM/SPF) received doses of 50, 100 and 200 mg/kg of the combination ASA+NAPAP+caffeine, 45 and 180 mg/kg of the combination ASA+NAPAP, and 50 and 200 mg/kg of the individual drugs ASA or NAPAP over a period of 6 months. The daily dose was splitted into two parts and administered 3 h apart. The rats were single housed under standardized conditions with free access to food and drinking water. Plasma concentrations were measured in four additional animals of all high dose groups after the last dosing at seven time points. Besides the usual routine toxicological investigations the kidneys of five females per group were investigated by transmission electron microscopy. All investigations were performed according to GLP regulations. All animals behaved unobtrusively throughout the study with only minor impairment of general conditions in some animals of all ASA, ASA+NAPAP+caffeine and the high dose NAPAP groups. Dose related mortality was observed in the groups receiving ASA alone or in combination, partly with rales and tonic convulsions immediately prior to death. Body weight gain was decreased in males but not in females of the ASA+NAPAP+ caffeine and ASA groups. No consistent drug- and dose-dependent changes in hematological, clinico-chemical or urinanalytical parameters were observed, except for a slight increase in excretion of epithelial cells in both genders of the ASA groups. Plasma drug level monitoring demonstrated that the pharmacokinetics of ASA were not altered by co-administration of caffeine or NAPAP or vice versa. In males, maximum plasma concentrations (Cmax) and areas under the curve (AUC) for ASA and NAPAP tended to be slightly lower than in females. The plasma concentrations reached in the study represent a low multiple (2.2-7.9) of therapeutic plasma levels. Therefore, the results reported in the study can be considered representative for normal therapeutic use of the analgesic combination ASA+NAPAP+caffeine. Gastric erosions in the ASA and ASA+NAPAP+caffeine groups, increased kidney weights in females given 200 mg/kg ASA+NAPAP+caffeine, and dose-dependently increased liver weights in females given 200 mg/kg ASA and decreased liver weights in males at 100 and 200 mg/kg ASA-NAPAP+caffeine were the only consistent drug-induced changes observed at necropsy. Except for the above mentioned ulcer, all histopathological findings were iatrogenic or spontaneous lesions. The kidneys demonstrated initial stages of age-associated nephropathy at comparable incidence and severity in all groups including controls. Semi-thin section evaluation and transmission electron microscopy showed only minor changes. Taking all tubular and vascular changes together (total mean), the animals of the NAPAP group were slightly more affected than those of the other groups. Summing up it can be concluded that the nephrotoxic potential of the combination ASA+NAPAP+caffeine, if existing at all, was marginal even after prolonged administration, and that it does not exceed that of the monosubstances when given at pharmacologically equipotent doses and clinically relevant exposures.

Acetaminophen↗

Time series analysis in critical care monitoring.

Time series analysis techniques facilitate statistical analysis of variables in the course of time. Continuous monitoring of the critically ill offers an especially wide range of applications. Several studies from different work groups show that autoregression, integration, moving average (ARIMA) models help to identify pathologic outliers and trends in physiologic variables in surgical critical care. The effect of therapeutic interventions on physiologic target variables has been estimated with interrupted ARIMA models. The time series before the therapeutic intervention were compared to changes under intervention using the same model including an intervention regressor. In most patients clinically relevant therapeutic effects could be statistically identified. Similarly, noneffective therapeutic maneuvers could be detected early, and eventually changes in therapeutic strategy initiated. These techniques appear to be most appropriate with electronic online measurements at short time intervals, e.g., heart rate, invasive pressures, regional oxygenation. But even on the basis of short time series of critical care monitoring variables, ARIMA models can successfully be employed for the analysis of laboratory variables and of therapeutic interventions. Nevertheless, due to high demands for manpower and to statistical methodological limitations, the general use of this methodology in clinical practice apart from controlled clinical studies cannot be recommended today. Nevertheless, time series analysis techniques bear a great potential for clinical applications. Ongoing studies will in the future allow us to apply time series analyses to a wide group of clinical problems. In clinical practice, time series analyses support a more analytical and reproducible approach toward the evaluation of pathologic changes and therapeutic effects in the individual patient. Present research focuses on the development of automatic methods for time series analysis that allow instantaneous statistical analysis at the bedside and algorithms for multivariate time series analysis. This would offer an option to the healthcare professional for a more reliable evaluation of the individual treatment. Therefore, it appears rewarding to invest further efforts into the development of medical time series analysis techniques.

Critical Illness↗

Two heads are better than one: crystal structure of the insect derived double domain Kazal inhibitor rhodniin in complex with thrombin.

Rhodniin is a highly specific inhibitor of thrombin isolated from the assassin bug Rhodnius prolixus. The 2.6 Angstrum crystal structure of the non-covalent complex between recombinant rhodniin and bovine alpha-thrombin reveals that the two Kazal-type domains of rhodniin bind to different sites of thrombin. The amino-terminal domain binds in a substrate-like manner to the narrow active-site cleft of thrombin; the imidazole group of the P1 His residue extends into the S1 pocket to form favourable hydrogen/ionic bonds with Asp189 at its bottom, and additionally with Glu192 at its entrance. The carboxy-terminal domain, whose distorted reactive-site loop cannot adopt the canonical conformation, docks to the fibrinogen recognition exosite via extensive electrostatic interactions. The rather acidic polypeptide linking the two domains is displaced from the thrombin surface, with none of its residues involved in direct salt bridges with thrombin. The tight (Ki = 2 x 10(-13) M) binding of rhodniin to thrombin is the result of the sum of steric and charge complementarity of the amino-terminal domain towards the active-site cleft, and of the electrostatic interactions between the carboxy-terminal domain and the exosite.

Amino Acid Sequence↗