Lignans from Trachelospermum jasminoides

Seven lignans having a diarylhydroxybutyrolactone skeleton were isolated from the leaves and stems of Trachelospermum jasminoides （Lindl.） Lem. Their structures were elucidated to be nortrachelogenin 8＇-O-beta-D-glucopyranoside （1）, nortrachelogenin 5 ＇- C- beta-D-glucopyranoside （2）, trachelogenin amide （3）, nortracheloside, trachelogenin, tracheloside, and trachelogenin 4＇- O- beta-gentiobioside, respectively, on the basis of spectroscopic analyses.     

mdx muscle pathology is independent of nNOS perturbation

In skeletal muscle, neuronal nitric oxide synthase (nNOS) is anchored to the sarcolemma via the dystrophin-glycoprotein complex. When dystrophin is absent, as in Duchenne muscular dystrophy patients and in mdx mice, nNOS is mislocalized to the interior of the muscle fiber where it continues to produce nitric oxide. This has led to the hypothesis that free radical toxicity from mislocalized nNOS may contribute to mdx muscle pathology. To test this hypothesis directly, we generated mice devoid of both nNOS and dystrophin. Overall, the nNOS- dystrophin null mice maintained the dystrophic characteristics of mdx mice. We evaluated the mice for several features of the dystrophic phenotype, including membrane damage and muscle morphology. Removal of nNOS did not alter the extent of sarcolemma damage, which is a hallmark of the dystrophic phenotype. Furthermore, muscle from nNOS-dystrophin null mice maintain the histological features of mdx pathology. Our results demonstrate that relocalization of nNOS to the cytosol does not contribute significantly to mdx pathogenesis.      

Nuclear genes of human complex I of the mitochondrial electron transport chain: state of the art

The mitochondrial electron transport chain (mtETC) consists of four multi-subunit enzyme complexes. Complex I or NADH:ubiquinone oxidoreductase, the largest mtETC multisubunit complex, consists of approximately 41 subunits. Seven of these subunits are encoded by the mitochondrial genome, the remainder by the nuclear genome. Among the mitochondriocytopathies, complex I deficiencies are encountered frequently. Although some complex I deficiencies have been associated with mitochondrial DNA mutations, the genetic defect has not been elucidated in the majority of complex I-deficient patients. It is expected that many of these patients have mutations in the nuclear- encoded subunits of this complex, so vital for cellular energy production. After a brief summary of the current knowledge of complex I from cow, bacteria and fungi, this review presents the state of the art of the knowledge of the human nuclear-encoded complex I genes which, in the last 18 months, has made enormous progress. At present, the complete gene structure of four subunits and the cDNA structure of 18 of the 34 complex I nuclear-encoded subunits are known. Mapping of these subunits shows a random distribution over the chromosomes. The chromosomal localization is known for 14 complex I genes. Recently, the first mutation, a 5 bp duplication in the 18 kDa (AQDQ) subunit, has been reported. We expect that within 1 year all human nuclear-encoded complex I subunits will be cloned. Mutational analysis of these subunits is warranted in complex I-deficient patients and will not only be important for genetic counselling but will also extend the knowledge regarding the functional properties of the individual human complex I subunits.      

Changes in EEG power density of NREM sleep in depressed patients during treatment with citalopram

According to a recent hypothesis the therapeutic effects of antidepressants might be related to acute or cumulative suppression of NREM sleep intensity. This intensity has been proposed to be expressed in the EEG power density in NREM sleep. In the present study the relationship was examined between the changes of EEG power density in NREM sleep and the changes in clinical state in 16 depressed patients during treatment with citalopram, a highly specific serotonin uptake inhibitor. A one-week wash-out period was followed by 1 week of placebo administration, a medication period of 5 weeks, and a one-week placebo period. In order to minimize systematic influences of sleep duration and NREM-REM sleep alterations, EEG power was measured over the longest common amount of NREM sleep stages 2, 3 and 4 (91.5 min). During the last treatment week and the week after withdrawal, a significant decrease of EEG power as compared to baseline was found in the 8-9 Hz frequency range. No clear-cut change, however, was observed in the EEG power of the delta frequency range (1-4 Hz), which is considered to be the principle manifestation of NREMS intensity. Furthermore, no relationship between changes in EEG power density and changes in clinical state could be demonstrated.     

Nutritional hazards of elimination diets in children with atopic eczema

The intake of nutrients over a five day period was studied in 23 children whose atopic eczema was being treated by the avoidance of multiple foods. The results were compared with those from 23 healthy control children not on a diet. Significantly low intakes of calcium were discovered in 13 patients but not in controls. Avoidance of multiple foods is potentially hazardous and requires continued paediatric and dietetic supervision.