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Biomedical subjects

A Hahn

Publications and source records attributed to A Hahn.

At least 37 records · Page 2Linked to original sources
PubMed2003

Gas adsorption in mcm-41 porous silicas dynamic measurements using SANS.

The isothermal gas adsorption of two hexane isomers (n-hexane and cyclohexane) in the mesopores of MCM-41 silica have been investigated by small angle neutron scattering (SANS). This has been achieved by performing SANS measurements under contrast matching conditions for the silica matrix and condensed hydrocarbon confined in the mesopores. Insight into the kinetics of adsorption have been derived from changes in the intensity of the (100) diffraction peak associated with the ordered hexagonal mesoporous structure of the MCM-41 silica.

Journal Article↗
PubMed2003

[Dietary supplements and functional food for weight reduction -- expectations and reality].

Looked at with scientific dispassion, much of the frequently aggressive advertising for slimming products must be considered to be dishonest and misleading. This applies, for example, to the "fat burner" carnitine or for chromium-containing preparations such as chromium picolinate, which in large doses have been shown to have detrimental effects on health. Products for which there actually is a scientific rationale all have minor weight-reducing effects, so that they must be considered to have at most an adjuvant role within the framework of evidence-based concepts for losing weight. Examples of alleged slimming substances that in reality can do no more than support weight reduction are the so-called medium-chain triglycerides (MCT) or caffeine, with the latter showing an effect vis-à-vis placebo only in combination studies with ephedrine.

Anti-Obesity Agents↗
PubMed2003

Endogenous CCK depresses contractile activity within the ascending myenteric reflex pathway of rat ileum.

The ascending excitatory reflex is an important part of the myenteric reflex. In order to study the ascending neural pathways, isolated segments of rat ileum were stimulated by electrical stimulation of the gut wall (20 V, 3 pulses per second, 1 ms) using platinum electrodes. The excitatory contractile response was recorded using perfused manometric side-hole tubing located 2 and 4 cm orally to the stimulation site. The contractile response to electrical stimulation was abolished by atropine (10(-6) M) or hexamethonium (10(-4) M). The excitatory response increased after administration of the cholecystokinin A (CCK(A)) receptor antagonists lorglumide (3x10(-6) M: +44.1%), devazepide (10(-8) M: +19.4%; 10(-7) M: +30.0%) and SR-27897 (10(-10) M: +21.8%, 10(-8) M: +47.0%, P<0.05, n=8). However, the CCK(B) receptor antagonist L-365,260 also caused a significant increase in the oral excitation (10(-6) M: +27.4%). sCCK-8 caused a significant reduction in the ascending response (10(-8) M: -11.5%) and induced spontaneously occurring contractions at doses ranging from 10(-10)-10(-6) M. CCK-9 significantly increased the ascending response (10(-7) M: +10.9%, P<0.05). However, caerulein (10(-10) M: -25.9%, 10(-8) M: -26.8%; P<0.01) and pentagastrin (10(-10) M: -20.2%, P<0.05; 10(-8) M: -23.7%, P<0.01; 10(-6) M: -28.3%, P<0.001) reduced the ascending contractile response significantly. These data, obtained with potent and highly specific CCK receptor antagonists, demonstrate an inhibitory role of endogenously released CCK within the ascending neural pathway. The data further suggest that exogenously applied CCK-related peptides have different effects on the myenteric reflex which might be due to excitation of the different involved neurons (short and long ascending inter- and motorneurons) in an unphysiological order. Thus in experiments investigating more complex neuronal circuits, experiments with antagonists should be regarded as more specific.

Animals↗
PubMed2003

Dietary intakes and lifestyle factors of a vegan population in Germany: results from the German Vegan Study.

OBJECTIVE: Evaluation of dietary intakes and lifestyle factors of German vegans. DESIGN: Cross-sectional study. SETTINGS: Germany. SUBJECTS: Subjects were recruited through journal advertisements. Of 868 volunteers, only 154 participated in all study segments (pre- and main questionnaire, two 9-day food frequency questionnaires, blood sampling) and fulfilled the following study criteria: vegan dietary intake at least 1 year prior to study start, minimum age of 18 y, no pregnancy or childbirth during the last 12 months. INTERVENTIONS: No interventions. RESULTS: All the 154 subjects had a comparatively low BMI (median 21.2 kg/m(2)), with an extremely low mean consumption of alcohol (0.77+/-3.14 g/day) and tobacco (96.8% were nonsmokers). Mean energy intake (total collective: 8.23+/-2.77 MJ) was higher in strict vegans than in moderate ones. Mean carbohydrate, fat, and protein intakes in proportion to energy (total collective: 57.1:29.7:11.6%) agreed with current recommendations. Recommended intakes for vitamins and minerals were attained through diet, except for calcium (median intake: 81.1% of recommendation), iodine (median: 40.6%), and cobalamin (median: 8.8%). For the male subgroup, the intake of a small amount of food of animal origin improved vitamin and mineral nutrient densities (except for zinc), whereas this was not the case for the female subgroup (except for calcium). CONCLUSION: In order to reach favourable vitamin and mineral intakes, vegans should consider taking supplements containing riboflavin, cobalamin, calcium, and iodine. Intake of total energy and protein should also be improved.

Adult↗
PubMed2001

Mutations in Kir2.1 cause the developmental and episodic electrical phenotypes of Andersen's syndrome.

Andersen's syndrome is characterized by periodic paralysis, cardiac arrhythmias, and dysmorphic features. We have mapped an Andersen's locus to chromosome 17q23 near the inward rectifying potassium channel gene KCNJ2. A missense mutation in KCNJ2 (encoding D71V) was identified in the linked family. Eight additional mutations were identified in unrelated patients. Expression of two of these mutations in Xenopus oocytes revealed loss of function and a dominant negative effect in Kir2.1 current as assayed by voltage-clamp. We conclude that mutations in Kir2.1 cause Andersen's syndrome. These findings suggest that Kir2.1 plays an important role in developmental signaling in addition to its previously recognized function in controlling cell excitability in skeletal muscle and heart.

Alleles↗
PubMed2001

Manganese, iron and sulfur K edge XAFS of promoted sulfated zirconia catalysts.

Promoted sulfated zirconia samples were prepared by the incipient wetness technique to produce isomerization catalysts which were active for the conversion of n-butane to isobutane at 338K (up to 10% conversion of 1% n-butane, 1atm., 0.25 h(-1) WHSV). The local structure of Fe and Mn in promoted sulfated zirconia was investigated using fluorescence yield XAS. Spectra were taken of calcined samples, activated samples, and samples after reaction with n-butane (maximum activity and deactivated). Factor analysis reveals that the Mn K edge XANES can be described by a linear combination of the spectra of two separate components, and that the ratio of these components changes with activation of the catalyst, and during use in the n-butane isomerization reaction. The change in ratio of the Mn species during activation and reaction results in a reduction of the average Mn valence from 2.4 to 2.2. The Fe K edge XANES was not similarly affected by activation and reaction with n-butane.

Journal Article↗
PubMed2001

Prevalence of donor-specific anti-HLA antibodies during episodes of renal allograft rejection.

BACKGROUND: Recent studies suggest that the appearance of anti-HLA antibodies in the early posttransplant period is associated with an increased incidence of acute and chronic rejection months later. However, very little is known about the prevalence of anti-HLA antibodies at the time that the rejection episodes are diagnosed. The purpose of this study was to analyze retrospectively 420 sera from 263 renal allograft recipients who were readmitted to the hospital for any reason between 1989 and 1998 in order to determine if a correlation existed between the presence of donor-specific anti-HLA antibodies and graft rejection. METHODS: Sera were assayed for IgG HLA class I and II antibodies by ELISA. The ELISA results were analyzed using contingency tables with Fisher's exact test and compared with mismatched antigens in the donor. RESULTS: Antibodies to donor HLA class I molecules in the posttransplant sera were extremely rare, occurring in only 6 of the 420 sera (1.4%) analyzed. Antibodies to donor class II antigens were slightly more common, occurring in 25 of the 420 sera (6%). In 21 of these 25 cases (84%), the presence of donor-specific HLA class II antibodies was associated with episodes of either acute (n=14) or chronic rejection (n=7). Five patients had antibodies to both class I and class II donor antigens, and all five of them lost their grafts to rejection. CONCLUSION: Although the presence of donor-specific HLA antibodies presented a significant risk for acute or chronic rejection, 77% of all acute and chronic rejections occurred in patients without detectable HLA antibodies.

Antibodies↗
PubMed2001

Laboratory signs of activated coagulation are common in Henoch-Schönlein purpura.

We investigated 17 patients with Henoch-Schönlein purpura (HSP) and describe as yet unreported abnormal results of blood coagulation tests. In parallel to the activity of the disease, D-dimer concentrations in plasma were found to be significantly increased in 15 of the 17 patients; almost 50% of all patients showed values higher than 10 times the upper limit of the normal range. In 11 patients, plasma concentrations of thrombin-antithrombin complex (TAT) and prothrombin fragments 1 and 2 (F1+2) were examined; six of them showed abnormal results. The pathologic values were correlated to the activity of the disease, but abnormalities were also found in milder cases of HSP. These findings probably reflect local reactions within inflamed blood vessels rather than a systemic activation of coagulation and hyperfibrinolysis. Clinicians should be aware of these laboratory findings in order not to confuse common cases of HSP with purpura necroticans, a very severe type of vasculitis in which signs of disseminated intravascular coagulation (DIC) have been reported. Our findings suggest that an activation of coagulation including hyperfibrinolysis secondary to the endothelial damage is a typical feature of the common types of HSP.

Antithrombin III↗
PubMed2001

Atypical "benign" partial epilepsy of childhood or pseudo-lennox syndrome. Part II: family study.

Atypical benign partial epilepsy of childhood (ABPE = Pseudo-Lennox syndrome) shows semiologic parallels to Lennox-Gastaut syndrome, however--besides the lack of tonic seizures--it has an entirely different etiology and prognosis. Recently Hahn et al [17] investigated the long-term evolution of 43 cases with ABPE. Symptomatology, EEG findings, and course were found to overlap with Rolandic epilepsy, Landau-Kleffner syndrome and ESES. The incidence of seizures in relatives was determined in the whole series investigated by Hahn et al [17]. Five of 56 siblings suffered from seizures (3 Rolandic seizures; one febrile convulsions; one unclassified). Three fathers reported grand mal. In 29 families of the series of Hahn et al EEG recordings were performed: 22 brothers, 19 sisters and 16 pairs of parents. In 29% of the siblings a sharp wave focus was demonstrable. The rate rose to 40% when only siblings investigated at the age of maximum expression (3 to 10 years) were considered. Sharp wave foci were mostly multifocal and indistinguishable from those observed in siblings of children with Rolandic epilepsy. Photoparoxysmal response and generalized spikes and waves during rest and hyperventilation were also found to be significantly elevated (26% and 13% respectively). We conclude that ABPE is a subgroup of idiopathic partial epilepsy of childhood (representing a less benign part of a spectrum) that has to be ranked in a continuum with Rolandic epilepsy. The different clinical phenotype might be caused by a higher expressivity of the identical genetic trait, possibly facilitated by other genetic or acquired factors. Genetic heterogeneity represents another possibility.

Adult↗
PubMed2001

Atypical "benign" partial epilepsy or pseudo-Lennox syndrome. Part I: symptomatology and long-term prognosis.

PURPOSE: Atypical benign partial epilepsy (ABPE) or pseudo-Lennox syndrome (PLS) is characterised by generalised minor seizures and focal sharp slow waves and spikes (SHW) as observed in Rolandic epilepsy (RE), but with exceptional pronounced activation during sleep. The aim of this study was to describe the full spectrum of ABPE in the hitherto largest group of patients. METHODS: We retrospectively analysed the clinical and EEG data of 43 children who fulfilled the following criteria: occurrence of generalised minor seizures as described for ABPE (i.e., atonicastatic seizures, myoclonic seizures, atypical absences) and focal SHW identical to those observed in RE, but with generalisation during sleep. RESULTS: Language development prior to onset of epilepsy was retarded in 26% of patients. In 74%, age at onset of epilepsy ranged from 2 to 6 years. Manifestation occurred earlier in boys than in girls. Generalised minor seizures constituted the predominating seizure type in 67% of patients. Twenty-eight percent of patients suffered from simple partial seizures of the oro-facial region or generalised tonic-clonic seizures originating from the oro-facial region. Additionally, generalised tonic-clonic (44%), unilateral (21%), partial motor (44%), versive (12%), focal atonic (9%), and complex-partial seizures (2%) were observed. A bioelectrical status was recorded in 56% of patients during sleep. No tonic seizures and no fast spike series (bursts of 10-20 Hz rhythms) were observed. At last follow-up, 84% of patients were in clinical remission. All subjects older than age 15 were seizure-free. However, 56% of patients attended a school for mentally handicapped children. CONCLUSIONS: ABPE or PLS broadly overlaps with RE, electrical status epilepticus during sleep, and Landau-Kleffner syndrome. Regarding the epilepsy, the prognosis is excellent, mental deficit, however, seems to be frequent. The differentiation from Lennox-Gastaut syndrome and myoclonic astatic epilepsy is essential. Instead of ABPE, the term pseudo-Lennox syndrome is proposed.

Cerebral Cortex↗
PubMed2001

Visuo-vestibular biofeedback in patients with peripheral vestibular disorders.

It is well known that diseases of the vestibular system can be compensated by increased spontaneous activity of other systems engaged in maintaining equilibrium, i.e. proprioceptive and visual systems. A complex approach using multisensory stimulation is the optimal way to achieve vestibular compensation. The aim of our study was to determine the effect of vestibular rehabilitation therapy as measured by posturography in a group of 72 patients suffering from vestibular disorders: Ménière's disease (n = 31), neuritis vestibularis (n = 21) and vertebrobasilar insufficiency (n = 20). Patients underwent the following examinations: electronystagmography; caloric, rotatory and optokinetic tests; computed posturography; craniocorpography; pure-tone audiometry; speech audiometry; and tinnitometry (tinnitus loudness, pitch). The instability in patients with Ménière's disease decreased 3 weeks after starting the therapy; nevertheless, the decrease in area (the surface formed by the movement of the patient's equilibrium point during a defined time) was transitory because of the increase in area values obtained between the 3rd and 6th weeks when measured with closed eyes. In the vestibular neuronitis patients, the measured values of area and the velocity of the patient's movement decreased continuously. The values measured in the patients suffering from vertebrobasilar insufficiency decreased continuously, the absolute values remaining pathological.

Adolescent↗
PubMed2001

Combined laser-EGb 761 tinnitus therapy.

The treatment of patients with chronic tinnitus is very problematic and therefore otologists are trying to discover more suitable courses of therapy. In this study we wanted to evaluate the outcome of using a combination of EGb 761 and soft laser therapy. We examined 120 patients with an average duration of tinnitus of 10 years. The patients underwent pure-tone audiometry, speech audiometry and objective audiometry tests. The intensity and frequency of tinnitus was also determined. EGb 761 was administered 3 weeks before starting soft laser therapy. Patients underwent 10 sessions of laser therapy, each lasting for 10 min. An improvement in tinnitus was audiometrically confirmed in 50.8% of patients: 10 dB in 18; 20 dB in 22; 30 dB in 10; 40 dB in 6; and 50 dB in 5.

Adolescent↗
PubMed2001

The clinical and laboratory features of chronic sensory ataxic neuropathy with anti-disialosyl IgM antibodies.

The clinical and laboratory phenotype of a paraproteinaemic neuropathy syndrome termed chronic sensory ataxic neuropathy with anti-disialosyl IgM antibodies is described in a series of 18 cases. Previous single case reports have outlined some features of this syndrome. All 18 cases were defined by the presence of serum IgM antibodies which react principally with NeuAc (alpha2-8)NeuAc(alpha2-3)Gal-configured disialosyl epitopes common to many gangliosides including GDlb, GD3, GTlb and GQlb. In 17 out of 18 cases, the serum contained benign IgM paraproteins, and in four of these cases at least two IgM paraproteins were present. The IgM antibodies were also cold agglutinins in 50% of cases. The clinical picture comprised a chronic neuropathy with marked sensory ataxia and areflexia, and with relatively preserved motor function in the limbs. In addition, 16 out of 18 cases had motor weakness affecting oculomotor and bulbar muscles as fixed or as relapsing-remitting features. When present in their entirety, these clinical features have been described previously under the acronym CANOMAD: chronic ataxic neuropathy, ophthalmoplegia, IgM paraprotein, cold agglutinins and disialosyl antibodies. This distribution of clinical features is reminiscent of Miller Fisher syndrome, in which acute-phase anti-disialylated ganglioside IgG antibodies are found. Clinical electrophysiology and nerve biopsy show both demyelinating and axonal features. A partial response to intravenous immunoglobulin and other treatments is reported in some cases.

Adult↗
PubMed2001

Regulation of connective tissue growth factor (ccn2; ctgf) gene expression in human mesangial cells: modulation by HMG CoA reductase inhibitors (statins).

AIM: Connective tissue growth factor (ccn; ctgf) gene expression is upregulated in fibrotic renal glomeruli. Therefore, the regulation and pharmacological modulation of ccn2 (ctgf) mRNA expression was investigated in a human renal mesangial cell line. METHODS: A human renal mesangial cell line was cultured in vitro under standard conditions. After stimulation, RNA was extracted and ccn2 (ctgf) mRNA expression assessed by northern blot analysis. RESULTS: The expression of ccn2 (ctgf) mRNA was transiently upregulated by fetal calf serum. Very rapid onset but short lasting ccn2 (ctgf) mRNA expression was observed after stimulation with lysophosphatidic acid, a bioactive lipid, which activates G protein coupled receptors. Induction of ccn2 (ctgf) mRNA expression by transforming growth factor beta (TGF-beta) was more prolonged and lasted for more than one day. The small GTPases of the Rho family were essential for basal as well as induced ccn2 (ctgf) expression: preincubation of the cells with toxin B from Clostridium difficile abrogated ccn2 (ctgf) mRNA expression. HMG CoA reductase inhibitors, which are therapeutically used as lipid lowering drugs, interfere with the isoprenylation and thus activation of Rho proteins. Simvastatin, an HMG CoA reductase inhibitor, inhibited ccn2 (ctgf) mRNA expression in a concentration dependent manner (IC(50): 1-2 microM). CONCLUSION: Statins were identified as potent inhibitors of ccn2 (ctgf) mRNA expression in mesangial cells, and therefore might be of potential use to modulate the excessive ccn2 (ctgf) expression in mesangial cells related to glomerular fibrosis.

Blotting, Northern↗
PubMed2000

Induction of connective tissue growth factor by activation of heptahelical receptors. Modulation by Rho proteins and the actin cytoskeleton.

Expression of connective tissue growth factor (CTGF) was induced in renal mesangial cells by activation of heptahelical receptors by serotonin (5-HT) and lysophosphatidic acid (LPA). Induction of CTGF mRNA was transient with maximal expression after 1 to 2 h, whereas induction of CTGF by transforming growth factor beta (TGF-beta) increased over time. In contrast to the induction of other early response genes (Egr-1 and cyclooxygenase-2), LPA-mediated induction of CTGF was pertussis toxin-insensitive and independent of p42/44 MAP kinase activation. 5-HT-mediated CTGF induction was due to activation of 5-HT(2A) receptors and likewise independent of p42/44 MAP kinase activation. Upon stimulation, enhanced levels of CTGF protein were detected in cellular homogenates, whereas no protein was detectable in cell culture supernatants. Inhibition of proteins of the Rho family by toxin B abrogated basal as well as CTGF expression stimulated by LPA, 5-HT, and TGF-beta. Inhibition of the downstream mediator of RhoA, the Rho kinase by Y-27632 partially reduced induction of CTGF by LPA and TGF-beta. Toxin B not only affected gene expression, but disrupted the actin cytoskeleton similarly as observed after treatment with cytochalasin D. Disassembly of actin stress fibers by cytochalasin D partially reduced basal and stimulated CTGF expression. These data indicate that an intact actin cytoskeleton is critical for the expression of CTGF. Elimination of the input of Rho proteins by toxin B, however, was significantly more effective and their effect on CTGF expression thus goes beyond disruption of the cytoskeleton. These findings thus establish activation of heptahelical receptors coupled to pertussis toxin-insensitive G proteins as a novel signaling pathway to induce CTGF. Proteins of the Rho family and an intact cytoskeleton were identified as critical determinants of CTGF expression induced by LPA and 5-HT, and also by TGF-beta.

Actins↗
PubMed2000

Endothelin b receptor deficiency is associated with an increased rate of neuronal apoptosis in the dentate gyrus.

The dentate gyrus retains neuronal proliferative potential throughout life. Using immature endothelin B receptor-deficient (sl/sl) rats, a rabbit model of pneumococcal meningitis and autopsy brains from humans who died from pneumococcal meningitis, we explored the role of endothelin B receptors in physiological and pathological neuronal apoptosis in the dentate gyrus. At postnatal days 3-4, the rate of apoptosis in the dentate gyrus was high in all rats, declining to low levels in wild-type rats (+/+) on days 14 and 22, but remaining high in both homozygous (sl/sl) and heterozygous (sl/+) endothelin B receptor-deficient rats. Increased apoptosis was not significantly compensated for by neuronal proliferation. Hippocampal neuronal cultures also exhibited genotype-dependent apoptosis with the highest rate in neurons from homozygous endothelin B receptor-deficient (sl/sl) rats. In rabbit and human pneumococcal meningitis, increased apoptosis in the dentate gyrus was associated with loss of neuronal endothelin B receptor immunoreactivity. In conclusion, endothelin B receptors appear to act as neuronal survival factors in the dentate gyrus in rodents and man, both during postnatal development and under pathological conditions.

Aging↗
PubMed2000

Differential glial and vascular expression of endothelins and their receptors in rat brain after neurotrauma.

We characterized the time-course, intensity of expression and cellular origin of components of the endothelin (ET) system in the rat brain after a standardized neurotrauma (cryogenic lesion of the parietal cortex). ET mRNAs were expressed at sham level after neurotrauma, whereas immunoreactivity for ET-1 was enhanced in glia and endothelium of the lesioned hemisphere and both hippocampi. The number of ET-3 positive mononuclear cells in the lesion perimeter increased starting at 24h after injury. At 48h after neurotrauma, ET-receptor immunoreactivity was increased in astrocytes. In basilar artery endothelium, ETB-immunoreactivity was reduced at 48h to 72h recovering at 7 days whereas ETA-receptor and ET-peptide immunoreactivities were not altered. In summary, neurotrauma leads to a multicellular stimulation of endothelins in the brain along with a delayed selective loss of vascular ETB-receptors. These changes seem to be posttranscriptional and cell type specific. They favor vasoconstriction increasing the risk of late vasospasm and ischemia.

Animals↗