Determination of the enantiomeric purity of (−−) 2-(N-propyl-n-2-thienylethylamino)-5-hydroxytetralin (n-0923) by chiral stationary phase HPLC

The determination of the enantiomeric impurity, i.e., the percentage of (+) N?0437 (= N?0924) in several batches of (??) N-0437 (= N-0923) by chiral HPLC is described. Enantiomeric impurities were calculated based on the peak areas of the two baseline separated enantiomers in the chromatogram. The enantiomeric impurities found in different batches ranged from 0.02% to 0.11%. Calibration curves of the two isomers of N-0437 (Fig. 1,) were made twice to study the reproducibility and linearity of the method. The absorbance ratio, N-0923/N-0924, was found to be 1.02 with a relative standard deviation (RSD) of 9% over the whole concentration range used for the calibration curves.     

The duplication in Charcot-Marie-Tooth disease type 1a spans at least 1100 kb on chromosome 17p11.2

Summary Recently, it has been shown that Charcot-Marie-Tooth disease type 1a (CMT1a) is linked with a duplication of a DNA segment that is detected by probe VAW409R3, and that is located on chromosome 17p11.2. Here, we show that this duplication also contains VAW412R3a, but not A10-41 and EW503. Accounting for the duplication in recombination analysis, we found recombinants between CMT1a and EW301 and EW502, but not with A10-41, VAW409R3, and VAW412R3. Using pulsed-field gel electrophoresis analysis, we estimated the minimal size of the duplicated region in CMT1a patients to be 1100 kb.     

Techniques for encapsulating bioactive agents into liposomes

As a prerequisite for the use of liposomes for delivery of biologically active agents, techniques are required for the efficient and rapid entrapment of such agents in liposomes. Here we review the variety of procedures available for trapping hydrophilic and hydrophobic compounds. Considerations which are addressed include factors influencing the choice of a particular liposomal system and techniques for the passive entrapment of drugs in multilamellar vesicles and unilamellar vesicles. Attention is also paid to active trapping procedures relying on the presence of (negatively) charged lipid or transmembrane ion gradients. Such gradients are particularly useful for concentrating lipophilic cationic drugs inside liposomes, allowing trapping efficiencies approaching 100%.     

Diversity of functional morphological explanation

An introduction to the 19th Lochmühle conference on Architecture in living structure, organized by P. Dullemeijer, W.F. Gutmann and G.A. Zweers, held from March 15–17, 1984 in the Aussenstelle des Forschungsinstituts Senckenberg der Senckenbergischen Naturforschenden Gesellschaft, Frankfurt am Main.     

Foraminifera from the Silberberg Formation («Lower Oligocene») at Silberberg,near Helmstedt (Germany)

From the Silberberg Quarry, type locality of the Silberberg Formation (Martini &Ritzkowski 1968), some planktonic foraminifera are described:Globigerina officinalis Subbotina, Globigerina ouachitaensisHowe &Wallace,G. praebulloides leroyi Blow &Banner, G.praebulloides occlusa Blow &Banner which taxa are here suggested to form intergrading morphotypes within the range of variation of a population dominated byG. officinalis. In addition,G. cf.danvillensis Howe &Wallace is found. The planktonic fauna, together with some elements in the benthonic fauna, suggests a possible correlation with the Danville Landing Member of the Jackson Formation, Louisiana, traditionally ascribed to the Upper Eocene. There is some similarity with European Uppermost Eocene — Lower Oligocene faunas described by various authors. The Silberberg Formation was suggested to be a Neostratotype for the Latdorfian Stage of the Lower Oligocene byMartini &Ritzkowski (1968). It is suggested that the Silberberg Formation may well be coeval with the Upper Priabonian as proposed byCita 1969.     

Biochemical Studies of Bacterial Sporulation and Germination XIV. Phospholipids in Bacillus megaterium

The principal phospholipids of Bacillus megaterium throughout the cycle of growth and sporulation were found to be phosphatidylglycerol, diphosphatidylglycerol, phosphatidylethanolamine, and a hitherto unidentified isomer of glycosaminyl-phosphatidylglycerol. Phosphatidylglycerol predominated during vegetative cell growth and then declined as spores developed, whereas diphosphatidylglycerol became more prominent during spore maturation. The latter phosphatide was relatively inaccessible in the vegetative cell and was more accessible in the spore, as judged by solvent extraction under various conditions.     

No evidence for ‘skewed’ inactivation of the X-chromosome as cause of Leber's hereditary optic neuropathy in female carriers

Leber’s hereditary optic neuropathy (LHON) is a maternally inherited disorder of the optic nerves. It has been proposed that the specific mutations in the mitochondrial DNA (mtDNA) that are associated with LHON require and X-chromosomally encoded permissive factor in order to become expressed. This would explain both the preponderance of male patients and the fact that most carriers of specific mtDNA mutations remain unaffected. Although linkage studies have been negative so far, the existence of such a factor has not been ruled out. We investigated the genealogical data of 24 large LHON pedigrees and concluded that the presumed X-linked factor would be recessively inherited and that at least 57% of the affected females would be heterozygous. Therefore, these females must be the victim of nonrandom X-chromosomal inactivation (skewed lyonization). However, analysis of X-chromosomal methylation patterns in 16 LHON-affected females revealed substantial skewing in only 15%–20% of cases, which is not significantly different from the patterns in 49 controls. Moreover, we found the frequency of LHON in daughters of affected heterozygous females to be twice to three times as high as in daughters of unaffected heterozygous females, which cannot be explained by an X-chromosomally inherited factor. We conclude that the results of our investigations do not support the hypothesis that LHON is a digenic disease with an X-linked factor being the main cause of loss of vision in the presence of relevant mtDNA mutations. Received: 1 June 1995 / Revised: 20 September 1995