Compression of the celiac trunk (author's transl)

Besides the vascular changes caused by arteriosclerosis the compression stenosis is the most frequent form of the isolated restriction of the arteria coeliaca. The compression of the arteria coeliaca, caused by the ligamentum arcuatum medianum or a fribromatous ganglion tissue, can cause complaints similar to the symptoms of angina abdominalis: pains in the epigastrium, postprandial pains, loss of weight, nausea/vomiting, diarrhea, 93% of the patients with severe vascular compression have an abdominal vascular murmur. Of 31 patients with angiographically proved compression stenosis, 11 patients suffering from occlusion or intense stenosis had to be operated because of heavy complaints. The angiographic and intraoperative findings allow the conclusion that there is a connection between the extent of the stenosis and the clinical appearance. The decompression of the arteria coeliaca, in other words the detachment of the compressing tissue leads to total complaintlessness in 83% of the patients. If the arteria coeliaca is hypoplastic a vessel widening or a bypass operation is necessary to establish normal blood circulation in the epigastric organs.     

Effect of long-term therapies with penicillin and sulfadiazine on Streptococcus mutans and lactobaccilli in dental plaque

Plaque samples were obtained from 13 children receiving long-term therapy with benzathine penicillin for the prevention of rheumatic fever recurrences, 31 children receiving oral sulfadiazine for the same purpose, and 29 untreated siblings. The therapies were found to have no effect upon the proportions of Streptococcus mutans or lactobacilli in dental plaque, upon the percentage of children harboring the organisms, nor upon the susceptibility of the organisms to penicillin and sulfadiazine. Of the S. mutans strains tested, 97% had a minimal inhibitory concentration of penicillin G of less than 48 ng/ml and, of the lactobacillus strains tested, 96.8% had a minimal inhibitory concentration of less than 1,600 ng/ml. All strains of both organisms were profoundly resistant to sulfadiazine.     

Correction of increased prostacyclin synthesis in Bartter's syndrome by indomethacin treatment

The role of prostacyclin and thromboxane A2 in the pathogenesis of Bartter's syndrome was investigated by measurement of the urinary excretion of 6-keto-PGF1 alpha and thromboxane B2, respectively, in five patients. The prostaglandin metabolites were extracted from urine by a reproducible method and measured by specific radioimmunoassays. The patients with Bartter's syndrome excreted about four-times as much 6-keto-PGF1 alpha as the normal controls. In contrast, there was no significant difference in the urinary excretion of thromboxane B2 between the patients and the controls. In a second part of the study, three patients were treated with indomethacin (150 mg/day for four days), an inhibitor of prostaglandin synthesis. This regimen suppressed urinary excretion of 6-keto-PGF1 alpha by 43% and that of thromboxane B2 by 46%. It is suggested that the increase in prostacyclin production is responsible for both the hyperreninemia and and the other endocrine derangements as well as the hyporesponsiveness of blood pressure to intravenous infusion of vasopressors in patients with Bartter's syndrome.     

Differential diagnostic question: traumatic unconsciousness or amnestic episode?

Traumatic twilight state on the one and amnestic episode (transient global amnesia) on the other side are as a rule easy to differentiate from the patient's age, his behavior during the acute state of disease and the kind of its improving. Contrary to other authors' opinion, differentiation is not just possible by diagnosing an injury or its absence. In minor skull traumata preceding the traumatic twilight states injuries are often not manifest and otherwise amnestic episodes occasionnally occur after minor traumata. In a 64 years old woman an obviously typical amnestic episode appeared in direct connection with a probable fall on the back of the head. A 28 years old man underwent a five-hour amnestic episode whereas the EEG showed normal curves. The episode occurred 15 minutes after striking hard upon the ground with the back of the head during a ground roll without following unconsciousness. In both cases traumatic twilight states were not involved. In account of the interval of 15 minutes the trauma of the second case seems not be be the direct cause for the manifestation of amnestic episode. It also shows that the aspect of the disease in the rare occurrence in younger or middle-aged persons is on principle not different from that in old ones. Since a special medical examination during the acute state is only possible as exception the patient's amnestically seizable behaviour obtains greatest importance in differential diagnosis. For the rare coincidence the trauma is given no pathogenetic relevance in amnestic episodes.     

Extracellular recordings from patterned neuronal networks using planar microelectrode arrays

Neuronal cell networks have been reconstructed on planar microelectrode arrays (MEAs) from dissociated hippocampal pyramidal neurons. Microcontact printing (microCP) and a photoresist-liftoff method were used to selectively localize poly-L-lysine (PLL) on the surface of MEAs. Haptotaxis led to the organization of the neurons into networks localized adjacent to microelectrodes. Various grids of PLL with 2-25-microm-wide lines spaced by 50-200 microm with 15-25-microm nodes at intersection points were used to guide cell body attachment and neurite outgrowth. Bursting activity with spike amplitude attenuation was observed, and multichannel recordings detected instances of coincident firing activity. Finally, we present here an extracellular recording from a approximately 2 microm bundle of guided neurites.