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Biomedical subjects

B Roth

Publications and source records attributed to B Roth.

At least 55 records · Page 3Linked to original sources

[Nephrocalcinosis in childhood. Sonographic findings and differential diagnosis].

Ultrasonography is the method of choice for the detection of medullary or cortical nephrocalcinosis in infancy and childhood. Compared with abdominal radiographs and computed tomography even smallest calcifications are detected more accurately. Using furosemide, ACTH, steroids or high doses of vitamin D, early forms of medullary nephrocalcinosis associated with a faint hyperechogenic rim at the margins of the renal pyramids can be diagnosed by ultrasound. Idiopathic hypercalciuria, Bartter's syndrome and renal tubular acidosis cause medullary nephrocalcinosis, whereas cortical nephrocalcinosis is the result of renal vein thrombosis; primary hyperoxaluria is associated with cortico-medullary calcifications. Due to the localisation of the nephrocalcinosis and the age distribution of the diseases, sonography merely enables us to narrow down differential diagnosis.

Aging

[Distal radius fracture; fixation using Kirschner wire or only a cast? A retrospective comparative study].

56 distal radius fractures were followed for a median period of 54 months (31-88 months) following the accident. Conservative treatment (immobilisation in a plaster alone) was compared to percutaneous K-wire fixation. The two groups of patients were matched in regard to type of fracture, age (+/- 5 years) and sex. The functional end result was assessed according to the scoring system of Gartland/Werley, which was modified by Solgaard. The operative treatment modality showed better functional end results, especially for intraarticular fractures, when compared to the conservatively treated fractures.

Aged

Effect of naloxone on diurnal polysomnographic manifestations of hypersomnia with sleep apnoea.

A simple blind study with small doses of naloxone (0.8-1.6 mg i.v.) was carried out in 11 patients with hypersomnia with sleep apnoea (HSA). The effect was studied by diurnal polysomnography. It was found that the administration of naloxone was followed by significant prolongation of wakefulness and by significant shortening of the total duration of the second stage of NREM sleep. The duration of the apnoeic episodes was also significantly shortened after naloxone, although their number did not alter. Increased activity of the endorphinergic system (which naloxone inhibits by receptor competition) evidently plays a role in the pathophysiology of HSA.

Adult

[Preliminary treatment of the recipient site and healing of open spongiosa transplant in post-traumatic osteitis].

On the occasion of a new surgical procedure 48 patients with chronic osteitis were treated with a new antiseptic called "Lavasept" and open spongiosa-treatment. The spongiosa-filling was covered with saturated Lavasept-dressing which were changed once or twice daily till the spontaneous wound-healing occurred. None of the 48 patients has shown complications of the wound-healing or a relapse till today.

Anti-Infective Agents, Local

[Naltrexone in narcolepsy. Initial experience].

The administration of 550 mg naltrexon in the course of 13 days did not four patients with narcolepsy-cataplexy to improvement of symptoms of the disease and did not improve their appetite or increase their body weight. No side-effects of naltrexon were observed.

Adult

The effect of naloxone on the symptoms of narcolepsy.

The effect of Naloxone (0.4 mg i.v.) was studied in 10 patients suffering from narcolepsy. The diurnal polysomnographic recordings showed that Naloxone leads to an increase in the latency of REM sleep (P less than 0.05), to a shortening of its total duration and to a decrease in the average amount of phasic manifestations in 1 min. of REM sleep (P less than 0.05). The Polygraphic sleepiness score for REM sleep decreased significantly (P less than 0.01). Naloxone led also to the disappearance of stages 3 and 4 NREM sleep, and to an increase in the total duration of stage 1 NREM sleep. Naloxone caused no change in the total performance in Bourdon's test; though it did enhance attention. There were no changes in the subjective perception of the state of arousal or of the psychomotor tempo. It was found no post-Naloxone alterations of blood pressure, body temperature, pulse or pupillary diameter. The above findings support the hypothesis that an hyperactive endorphinergic system participates in the pathophysiology of narcolepsy.

Adult

Monoclonal antibodies to the main immunogenic region of the nicotinic acetylcholine receptor bind to residues 61-76 of the alpha subunit.

Monoclonal antibodies (mAbs) to the main immunogenic region (MIR) bind to fusion proteins containing region 37-200 of the alpha chain of Torpedo, mouse, and chicken nicotinic acetylcholine receptor. In the case of the mouse alpha chain, these mAbs react with sequence 61-216 but not with 74-216. A synthetic peptide M1, containing residues 61-76 of the mouse alpha chain, also binds these anti-MIR mAbs, showing that all or part of their binding site is included in this region. The conformational dependence and epitope specificity of the mAbs are discussed.

Amino Acid Sequence

Glucocorticoid receptors in mononuclear blood cells and their correlation to endogenous and exogenous corticoids in healthy and asthmatic children.

The number and affinity of glucocorticoid binding sites in peripheral mononuclear cells (MNC) of asthmatic and healthy children were determined by a whole cell (3H)dexamethasone binding assay at 37 degrees C. Using HPLC determination, corresponding serum levels of non-protein-bound (free) cortisol, whole cortisol and cortisone as well as urine excretion of free cortisone and cortisol were assessed. The average number of binding sites (BS) per cell and the dissociation constant (KD) respectively, in atopic asthmatics (7768 +/- 666 BS/MNC resp. KD = 17.2 +/- 2 nM) did not differ from the values measured in our control group (8333 +/- 691 BS/MNC resp. 25.4 +/- 4.8 nM). Within the age range 1 month-15.8 years neither age-dependent changes nor sex-related differences in the number of binding sites or the KD values could be detected. Active or currently inactive asthmatics, and patients under different antiasthmatic drug regimes, had similar binding sites on MNC. No differences in serum levels of cortisol, cortisone and free cortisol or in free cortisol and free cortisone of 24-h urine samples were found between healthy children and asthmatics. After a short course of prednisolone therapy for an acute severe asthmatic attack the number of glucocorticoid binding sites in peripheral MNC decreased to an average of 4632 +/- 421 BS/MNC, whereas the dissociation constant did not change significantly (14.5 +/- 3.6 nM). The corticoid-hormone pattern in the serum, 24-h urine excretion, and the normal number and affinity of glucocorticoid receptors on peripheral MNC suggest that there is no primary, general impairment of glucocorticoid metabolism in asthmatic children.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

Di-(2-ethylhexyl)-phthalate as plasticizer in PVC respiratory tubing systems: indications of hazardous effects on pulmonary function in mechanically ventilated, preterm infants.

Several PVC medical devices contain the plasticizer Di-(2-ethylhexyl)-phthalate (DEHP) in high concentration. Taken systematically DEHP only has minor toxic effects in the human organism. In three preterm infants artificially ventilated with PVC respiratory tubes unusual lung disorders resembling those observed in hyaline membrane disease, verified both clinically and radiologically, were observed during the fourth week of life. It was assumed that these lung disorders were causally related to the exposure to high doses of DEHP, which was released from the walls of the respiratory tubes. DEHP was found in the lung tissue of one patient who died of pneumothorax soon after birth after being artificially ventilated. It is strongly recommended that for disposable PVC respiratory devices the plasticizer DEHP should be used with more restrictions.

Diethylhexyl Phthalate

2,4-Diamino-5-benzylpyrimidines and analogues as antibacterial agents. 9. Lipophilic trimethoprim analogues as antigonococcal agents.

Lipophilic analogues of trimethoprim (1) bearing 3,5-dialkyl-4-hydroxy substituents in the benzene ring are much more active in vitro against Neisseria gonorrhoeae than is 1. The 3,5-diisopropyl-4-hydroxy derivative (2) was selected as a candidate for clinical evaluation as an antigonococcal agent, and as part of the preliminary evaluation it was submitted to extended pharmacokinetic and metabolism studies in dogs. Although the compound was not extensively conjugated by metabolic enzymes, one of the methyl groups was metabolized to produce a 3-isopropyl-4-hydroxy-5-(alpha-carboxyethyl)benzyl derivative (43), which was rapidly excreted. Related analogues were likewise extensively metabolized.

Animals

A study of the occurrence of HLA DR2 in 124 narcoleptics: clinical aspects.

The authors examined HLA antigens in 124 narcoleptics. In addition to narcolepsy, 122 patients suffered also from cataplexy. The two patients without cataplexy suffered also from sleep paralysis and hypnagogic hallucinations. These two symptoms were also present in many of the other patients. HLA group DR2 was found in 120 patients including all six symptomatic cases. In four patients HLA DR2 was not present. Two of these were fully pronounced narcolepsy-cataplexy cases whereas the two other did not suffer from cataplexy. Since several other cases with negative DR2 have already been published it is necessary to admit the existence of DR2-negative narcolepsy, albeit very rare. Among 5 patients with isolated sleep paralysis HLA DR2 was present in one familial and 1 sporadic case. The authors further discuss some aspects of the classification of narcolepsies in the light of recent HLA studies as well as their delimitation from idiopathic hypersomnia.

Cataplexy

BAEPs in hereditary motor-sensory neuropathies. Involvement of central brain-stem parts of the auditory pathway.

Brain-stem auditory evoked potentials (BAEPs) were tested in 34 patients with hereditary motor and sensory neuropathy (HMSN), most of which with HMSN type I with the autosomal dominant type of inheritance. In only a few cases a recessive or sporadic form of the disease was diagnosed, and one patient was rated as HMSN type III. In 44% complicated forms with signs of CNS involvement (cerebellar manifestation, nystagmus or cranial nerve lesions) were ascertained. BAEPs tests revealed slightly, albeit non-significantly prolonged wave III latency while wave V latency was significantly prolonged and so was the interpeak interval of waves III-V. One third of the records showed a prominent decrease in wave V amplitude.

Adolescent

Kleine-Levin syndrome ethiopathogenesis and treatment.

The complex of the symptoms of psychic disorders and of the disorders of sleep, appetite, and food intake often forms the basis of the clinical picture of a mental disease. However, it is only rarely conceived in a complex manner as a set of physiologically interdependent functions. A remarkable proof of the interdependence of these functions is their complex disorder, the Kleine-Levin syndrome. The first descriptions of the symptoms of the Kleine-Levin syndrome can be found in the studies of several authors published as early as at the turn of the century. In 1942, the syndrome was designated by Critchley and Hoffmann after Willi Kleine and Max Levin, who defined it precisely in 1925 and 1929. The syndrome of periodic hypersomnia, megaphagia, and psychic disorders, originally described only in young males, was later found in females as well; the original very strict criteria were gradually broadened and complemented to some extent. At present, the most commonly accepted criterion for the diagnosis of the Kleine-Levin syndrome is the existence of the combined sleep disorder (hypersomnia or insomnia lasting from days to weeks), food intake disorders (megaphagia or anorexia), and various psychic abnormalities accompanying or following the attacks of the affection. We term the syndrome typical if the sleep disorder appears in the form of hypersomnia, food disorder in the form of megaphagia, and if psychic abnormalities are clearly expressed. On the other hand, we term the syndrome atypical if one of the main symptoms is opposite. The incomplete syndrome consists of only two main symptoms. The attacks of the affection set on mostly suddenly, lasting from several days to several weeks, ending suddenly again. The interparoxysmal periods last from several days to several months, sometimes even to several years. The etiopathogenesis of the affection is still unknown. A number of reports indicate a disorder of the diencephalon, perhaps only of the hypothalamus. The pathological-anatomical findings following the death of persons suffering from the disorders of sleep and food intake and from psychic abnormalities mostly reveal lesions in the region of the third brain ventricle. The development of the typical syndrome is benign, however, and morphological studies are not available. The typical Kleine-Levin syndrome can hardly escape the attention of clinicians owing to the richness and clarity of symptoms. The atypical or discretely expressed forms, however, often remain unrecognized even after a detailed medical examination and may lead to diagnostic uncertainty.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult

Exogenous enzymatic modulation of lectin binding sites in human tissue. Development of hemolysis in hemolytic-uremic syndrome (HUS) considering alteration of the glycocalyx in the erythrocyte membrane.

FITC-labelled lectins (DBA, PNA, RCAI, UEAI) with different carbohydrate specificity were used to look for possible alterations of the glycocalyx of erythrocyte membrane in patients with hemolytic uraemic syndrome (HUS; n = 34) in comparison with controls (n = 66). These investigations revealed that patients with the blood group A, B and O possess a significantly higher amount of sialic acid covered binding sites for PNA (p less than 0.05) on the membrane of red blood cells than controls, as measured by quantitative fluorescence microscopy. This significant difference was additionally found for sialic acid substituted RCAI binding sites on B erythrocytes (p less than 0.05). Without pretreatment of red blood cells with neuraminidase a significant difference between HUS patients and controls was observed for PNA on A, for RCAI on O and for UEAI on A erythrocytes. The measured values are influenced by contamination of red blood cells with serum glycoproteins as could be assessed by the lower values on washed erythrocytes. As a whole the results indicate that the composition of the glycocalyx in red blood cells of HUS patients seems to be altered and that the pathogenesis of this syndrome is additionally influenced by serum factors. With the exception of UEAI that possesses a significant higher amount of binding sites on washed erythrocytes of blood group O the other lectins used are not suitable for the demonstration of blood group specificity.

Blood Group Antigens

Interaction of the antifolate antibiotic trimethoprim with phosphatidylcholine membranes: a 13C and 31P nuclear magnetic resonance study.

The interaction of the bacterial dihydrofolate reductase inhibitor trimethoprim with small unilamellar 1,2-dimyristoyl-sn-glycero-3-phosphorylcholine vesicles was studied using 13C and 31P NMR spectroscopy. In an effort to determine whether trimethoprim passively permeates the vesicle membrane, an impermeant, anionic complex of the paramagnetic ion Dy3+ was added to the extravesicular compartment. Based on the downfield shift that the Dy3+ complex induces in the [2-13C] resonance of trimethoprim in free solution, membrane permeation and movement of the drug into the intravesicular space can in principle be established from observation of the C2 chemical shift alone. In contrast to what is predicted by a two-compartment model separated by a semipermeable barrier, the presence of vesicles virtually reverses the effect of the shift reagent on the [2-13C] carbon resonance. These results suggest that the majority of the trimethoprim might be sequestered within the vesicle membrane. A saturable decrease in the spin-lattice relaxation time and a saturable increase in the line width at half-height of the [2-13C] resonance as a function of vesicle concentration indicated that trimethoprim does in fact bind to the phospholipid matrix of the membrane bilayer. The KD for the interaction calculated from the relaxation data was 9.7 +/- 0.3 X 10(-4) M at a pH of 7.01 and an ionic strength of 0.015 M. The chemical shift of the [2-13C] resonance is unaffected by interaction with the electroneutral membrane, and the pKa increases by only 0.16 upon binding. These results point to an interfacial location for the pyrimidine moiety. Using the paramagnetic shift reagent Pr3+ and the 31P NMR signal from the phosphodiester groups of the membrane lipids, trimethoprim was shown to displace Pr3+ ions from binding sites on the outer membrane surface as would be expected if the polar pyrimidine ring were located at or near the membrane surface. The extent to which trimethoprim and trimethoprim derivatives modified in the 3'- and 4'-positions interact with the exo face of the membrane is strongly dependent on the type of substituent and whether it is in the 3'- or 4'-position. Van der Waals interactions between the 5-benzyl sidechain and the hydrophobic fatty acid region of the membrane interior appear to be necessary for the polar portion of trimethoprim to compete favorably for the membrane-binding site with the polyvalent Pr3+ ion.(ABSTRACT TRUNCATED AT 400 WORDS)

Cell Membrane Permeability