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Biomedical subjects

M Claussen

Publications and source records attributed to M Claussen.

30 records · Page 2Linked to original sources

[Modification of nonspecific bronchial hyperreactivity to cold air hyperventilation and carbachol by nedocromil and budesonide].

In a double blind crossover trial we compared the effect of a four week treatment with inhaled nedocromil (4 x 4 mg/d) or budesonide (2 x 400 micrograms/d by spacer) on non-specific bronchial hyperresponsiveness (BHR) to cold air hyperventilation (CHV) and carbachol. 15 persons with clinically mild asthma, who showed a more than 50% decrease in sG(aw) after CHV were randomly allocated to treatment groups. A double dummy technique was applied. Before and after both treatment periods, which were separated by an out wash period of four weeks, BHR to isocapnic cold air hyperventilation and carbachol was determined on two consecutive days. 13 persons completed the study. Maximum percentual drop of sG(aw-) and FEV1-values after CHV, the number of steps of carbachol-provocation carried out to reach a decrease in sGaw of at least 50% and the calculated cumulative breath units (CBU) of carbachol to cause a 50% (20%) decrease in sG(aw) (FEV1) were assessed. Peak-flow values were registered throughout the study. Data were compared by means of Wilcoxon's matched-pairs signed-ranks test. After budesonide most parameter showed a significant decrease of BHR (CHV: sG(aw) p < 0.1; FEV1 p < 0.05; Carbachol: provocation-steps: p < 0.05; CBU: PD50 sG(aw) p < 0.05; PD20 FEV1 p < 0.05). There was no evidence for an influence of nedocromil on BHR (p-values all > 0.2). Comparing both treatments there was a difference in favour of budesonide partly reaching significance at 5% level. Budesonide but not nedocromil treatment showed a significant increase in peak-flow values (morning p < 0.02, evening p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Incidence of neuronal ceroid-lipofuscinoses in West Germany: variation of a method for studying autosomal recessive disorders.

The incidence of neuronal ceroid-lipofuscinoses (NCL) in West Germany was determined using a novel method which is applicable to other autosomal recessively inherited diseases. Questionnaires were sent to all pediatric departments (answer rate 189/276, 68%), schools for the blind (39/46, 85%), and neuropathological institutes (15/22, 68%). Diagnoses were accepted only when based on firm clinical and/or electron microscopic criteria; 207 such identified patients were sorted according to year of birth. Plotting the cumulative number of new cases per year against the year of birth resulted in a slightly S-shaped curve. Before the year 1962, the curve is relatively flat, probably due to inefficient case registration. Between 1968 and 1977, the slope of the curve is constant--a steep, nearly straight line. Thereafter the curve flattens out again, likely due to inefficient registration of young, still undiagnosed patients. We interpret the central segment of the curve, which is continuously straight over a period of 10 years and corresponds to 92 patients, as a period in which efficient registration of new cases occurred. The number of live births being 7,211,543 during the same period, the NCL incidence is calculated to be 1.28 per 100,000 live births (0.71 for juvenile NCL and 0.46 for late infantile NCL).

Child↗

Development and perinatal risk factors of very low-birth-weight infants. Small versus appropriate for gestational age.

371 long-term surviving very low-birth-weight (VLBW) infants born between July 1983 and June 1986 with a birthweight under 1501 g were followed-up. This sample amounted to 91% of such infants of six neonatal intensive care units in Hamburg (Germany). A neurological examination and a developmental evaluation using the Griffith Developmental Scale were carried out at the age of 18 to 20 months, corrected for gestational age. Ninety-six of the 371 infants were small for gestational age (SGA), 275 appropriate for gestational age (AGA). Striking differences between these two groups were found concerning perinatal risk factors and neurological outcome. Maternal risk factors associated with intrauterine growth retardation such as maternal toxemia and signs of fetal stress were found in a high percentage of the mothers of SGA-children, factors associated with premature labor and chorioamnionitis in mothers of AGA-children. Cerebral palsy was detected in only 7% of the SGA-children but 17.5% of the AGA-children. The difference in the development of cerebral palsy was attributed mainly to different postconceptual ages of the SGA- and AGA-children. In general, minor neurological abnormalities were detected in as many as 30% of SGA- and only 15.3% of AGA-children. None of the SGA-children over 33 weeks of gestational age developed cerebral palsy, but 25% minor neurological abnormalities. As to cerebral palsy the prognosis of SGA-infants with a very low birthweight is not different from AGA-infants with a similar gestational age. Regarding the development of minor neurological abnormalities, however, intrauterine growth retardation seems to be a risk factor independent from gestational age.

Attention Deficit Disorder with Hyperactivity↗

Development of very low birth weight infants: a regional study of 371 survivors.

We re-examined 371 infants with birth weights less than 1501 g at a corrected age of 18-20 months. This sample amounted to 91% of such infants admitted to one of the six neonatal intensive care units in Hamburg between July 1983 and 1986. The neurological examination and a developmental evaluation using the Griffith Developmental Scale revealed higher rates of abnormalities than in most other studies. Fifty-five children (14.8%) suffered from cerebral palsy, classified in 45 as spastic diplegia, in 5 as spastic tetraplegia, in 1 as spastic hemiplegia and in 4 as dystonia. Of the children, 41 (11%) showed minor neurological deviations (hyperactivity, clumsiness, intention tremor). The development of 30 children (8%) without neurological abnormalities was moderately retarded (DQ 80-89, corrected for gestational age [GA]). Nineteen children (5%) were severely retarded (DQ less than 80, corrected for GA) and four children (1.5%) were blind due to retrolental fibroplasia. An isolated delay of speech development was found in 5 children. Seventy children (18.9%) had a major and 87 children (23.5%) a minor handicap.

Cerebral Palsy↗

Effects of membrane lipid and fluidity modifications on HIV-1 infectibility of primate lymphocytes in vitro.

Although most non-human primates, except the chimpanzee and the gibbon in vivo are not infectible by HIV-1, lymphocytes of several of these species can be infected by HIV-1 in vitro. In order to investigate whether the in vitro infectibility of primate lymphocytes might be attributed to plasma membrane adaptation processes or to serum factors, we compared HIV-1 infectibility of cultivated peripheral blood lymphocytes of macaques and of baboons on day one and on day ten of cultivation. These data were correlated to plasma membrane lipid composition and membrane fluidity. We found a correlation between increased HIV-1 in vitro infectibility and changes in plasma membrane lipid composition resulting in decreased membrane fluidity of cultured primate lymphocytes.

Animals↗

Decreased plasma membrane fluidity of peripheral blood lymphocytes after diethyldithiocarbamate (DTC) therapy in HIV-infected patients.

In seeking the putative mechanism of action of diethyldithiocarbamate (DTC) on the immune status of HIV infected patients, the plasma membrane fluidity of peripheral blood lymphocytes (PBL) from DTC-treated and untreated patients (CDC III-IVc1) was determined. Anisotropy values of the fluorescent probe 6-(9-anthroyloxy) stearic acid were increased in DTC-treated patients (0.175 vs 0.161), indicating decreased PBL plasma membrane fluidity. The membrane rigidifying effect was significantly greater 4 h after i.v. drug administration (0.185 in treated patients). As the membrane fluidity and the function of membrane embedded antigen are interdependent, it is possible that alterations in biophysical and/or biochemical properties of membranes may account for the beneficial effect of DTC on the immune function and clinical status of HIV infected patients.

Acquired Immunodeficiency Syndrome↗

Increased plasma membrane fluidity and decreased receptor availability of nonmuscle cells in myotonic dystrophy.

Plasma membrane fluidity of intact nonmuscle cells from patients with myotonic dystrophy (MyD) was determined by fluorescence anisotropy measurements. Anisotropy values of the probe diphenylhexatriene were decreased in patient mononuclear cells (0.163 +/- 0.017, n = 13) versus controls (0.181 +/- 0.013, n = 13, P less than 0.01) and in patient platelets (0.087 +/- 0.017, n = 9) versus controls (0.137 +/- 0.015, n = 9, P less than 0.001) indicating increased plasma membrane fluidity in patient nonmuscle cells. Vasopressin plasma concentrations were increased in patients (7.4 +/- 2.1 pg/ml, n = 12) versus controls (4.5 +/- 1.4 pg/ml, n = 22, P less than 0.0005), whereas serum osmolality was normal. These data are compatible with a decreased vasopressin sensitivity in MyD patients. Specific binding of 125I-labelled vasoactive intestinal peptide (VIP) was decreased in patient mononuclear cells (2.9 +/- 0.9%/10(6) cells, n = 8) versus controls (5.2 +/- 1.6%/10(6) cells, n = 9, P less than 0.005) and receptor affinity for VIP was decreased in patient mononuclear cells (Kd = 0.26 +/- 0.05 nM, n = 8) versus controls (Kd = 0.19 +/- 0.02 nM, n = 9, P less than 0.005). In nonmuscle cells of MyD patients, increased membrane fluidity correlated with decreased receptor availability. This might explain the various endocrine defects described in MyD patients.

Adolescent↗

A membrane fluidizing factor in sera from Duchenne muscular dystrophy patients: effect on lymphocyte membranes of incubation in patient and control lipoproteins.

Sera from Duchenne muscular dystrophy (DMD) patients showed a membrane fluidizing effect on DMD and control lymphocytes. To look for the cause of this membrane fluidizing effect, human lymphocytes from healthy subjects were incubated in sera and in different serum fractions from DMD patients and healthy control subjects, and membrane fluidity was determined by steady state fluorescence polarization of the probe diphenyl hexatriene. DMD sera and total DMD lipoproteins showed a similar membrane fluidizing effect (p less than 0.02) after incubation, whereas lipoprotein deficient serum did not show any effect on membrane fluidity. Control and DMD HDL showed a membrane fluidizing effect, the fluidizing effect of DMD HDL being slightly higher as compared to control HDL. Control LDL and DMD LDL showed a membrane rigidifying effect, the rigidifying effect of DMD LDL being significantly lower as compared to control LDL (p less than 0.02). These data demonstrate that the membrane fluidizing effect of DMD serum is lipoprotein associated, LDL being the most important mediator of this effect.

Adolescent↗

Membrane fluidity and lipid composition of rat small intestinal brush-border membranes during postnatal maturation.

Fluidity and lipid composition of rat small intestinal brush-border membranes (BBM) were studied during maturation in five age groups: newborns, sucklings (1-3 weeks), weaned (4-6 weeks), juveniles (8-10 weeks), and adults (12 weeks). Brush-border membrane fluidity was measured by steady-state fluorescence polarization. Fluorescent probes used were: 1,6-diphenyl-1,3,5-hexatriene, 1-(4-trimethylammonium)phenyl)-6-phenyl-1,3,5-hexatriene, and a set of n-(9-anthroyloxy) fatty acids. Fluorescence anisotropy measured with all fluorophores was increased in adult versus newborn rats (P less than 0.004). The weight ratio of saturated to cis-unsaturated fatty acids increased from birth to the suckling age (P less than 0.0004). The cholesterol to phospholipid molar ratio increased from birth to the weaned age (P less than 0.0001). Cholesterol to protein ratio and phospholipid to protein ratio decreased after the weaned age (P less than 0.004). The results not only describe maturational changes of brush-border membranes but also give a better understanding of the correlations between biophysical and biochemical data in biological membranes.

Animals↗

Biodegradation of phenylbenzoate and some of its derivatives by Scedosporium apiospermum.

Scedosporium apiospermum, a recently isolated phenol-degrading hyphomycete, was shown to be able to productively utilise the diaryl ester phenylbenzoate as its sole source of carbon and energy. The characterisation of degradation intermediates together with the detection of the corresponding catabolic enzymes in crude extracts enabled us to propose a pathway for the degradation of this diaryl ester. According to our results, an inducible esterase initiated the biodegradation of phenylbenzoate by hydrolysing the ester bond to yield stoichiometric amounts of phenol and benzoate. While phenol was catabolised via catechol and hydroxyhydroquinone, the benzoate was further degraded via the protocatechuate branch of the ortho-pathway. In addition, the fungus utilised p-tolylbenzoate and 4-chlorophenylbenzoate by employing similar catabolic sequences.

Benzoates↗

[Homozygous alpha-1 antitrypsin deficiency (PiZZ) and bronchial asthma in childhood--is there a connection?].

Ten children and adolescents (aged four to 21 years) with the homozygous form of alpha-1-antitrypsin deficiency (PiZZ) were investigated with regard to obstructive airway disease. Besides the recording of the history, tests of lung function and allergy tests were performed. It was shown that bronchial asthma occurred in three out of ten patients. However, we could not demonstrate any statistically significant increased incidence of bronchial asthma in our unselected PiZZ-patients compared to the overall population. There was no indication of emphysema in any of the nine patients.

Adolescent↗

In vitro susceptibilities of enterococcal blood culture isolates from the Hamburg area to ten antibiotics.

Treatment of enterococcal infections is often difficult because of intrinsic and acquired resistance to a variety of antimicrobial agents. Between January 1993 and May 1997, enterococci were isolated from blood cultures of 117 patients at the Institute of Medical Microbiology and Immunology, University Hospital Eppendorf, Hamburg, Germany. Eightynine (76%) isolates were phenotypically identified as Enterococcus faecalis, and 24 (21%) as Enterococcus faecium. All E. faecalis isolates, but only 17% of the E. faecium isolates were susceptible to ampicillin. Two E. faecium isolates (8%) but no E. faecalis were vancomycin resistant (vanA genotype). Quinupristin/dalfopristin shows a high degree of susceptiblity of E. faecium (79%) and may be suitable for the therapy of infections caused by glycopeptide-resistant E. faecium strains.

Aged↗