Preliminary observations of a bacteriophage infectingXenorhabdus luminescens (Enterobacteriaceae)

A bacteriophage infective toXenorhabdus luminescens, a bacterial symbiont of heterorhabditid nematodes, was recovered from insects that supported poor nematode development. Plaque tests showed the phage particles to be infective only to primary and not secondary colonies ofX. luminescens. The phage was not infective toX. nenatophilus primaries or secondaries. The bacteriophage particles ranged 80–90 nm in length, with the head ranging from 40 to 50 nm in diameter. Restriction analysis was performed on isolated bacteriophage DNA. This first report of a bacteriophage fromXenorhabdus species has pratical implications since it could be detrimental to cultures ofHeterorhabditis nematodes that are being produced throughout the world for the biological control of insects.     

Human immunodeficiency virus induces phosphorylation of its cell surface receptor

AIDS is an immunoregulatory disorder characterized by depletion of the CD4+, helper/inducer lymphocyte population. The causative agent of this disease is the human immunodeficiency virus, HIV, which infects CD4+ cells and leads to cytopathic effects characterized by syncytia formation and cell death. Recent studies have demonstrated that binding of HIV to its cellular receptor CD4 is necessary for viral entry. We find that binding of HIV to CD4 induces rapid and sustained phosphorylation of CD4 which could involve protein kinase C. HIV-induced CD4 phosphorylation can be blocked by antibody against CD4 and monoclonal antibody against the HIV envelope glycoprotein gp120, indicating that a specific interaction between CD4 and gp120 is required for phosphorylation. Electron microscopy shows that a protein kinase C inhibitor does not impair binding of HIV to CD4+ cells, but causes an apparent accumulation of virus particles at the cell surface, at the same time inhibiting viral infectivity. These results indicate a possible role for HIV-induced CD4 phosphorylation in viral entry and identify a potential target for antiviral therapy.     

In vitro associations of tomato plants andRhizobium; induction of nitrogenase activity

Summary In vitro associations of the non-legumeLycopersicum esculentum andRhizobium sp. cowpea 32H1 were established. Tomato plants induced rhizobial nitrogenase activity. Induction of nitrogenase activity was possible through a membrane which was impermeable for bacteria.     

The biosynthesis of 6-azauracil riboside byEscherichia coli growing in the presence of 6-azauracil

Zusammenfassung Bei der Kultivierung vonE. coli in 6-azaurazilhaltigem Medium wird ein neuer Stoff akkumuliert, der als 6-Azaurazilribosid identifiziert wurde.     

Cardiac angiogenic imbalance leads to peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM) is an often fatal disease that affects pregnant women who are near delivery, and it occurs more frequently in women with pre-eclampsia and/or multiple gestation. The aetiology of PPCM, and why it is associated with pre-eclampsia, remain unknown. Here we show that PPCM is associated with a systemic angiogenic imbalance, accentuated by pre-eclampsia. Mice that lack cardiac PGC-1α, a powerful regulator of angiogenesis, develop profound PPCM. Importantly, the PPCM is entirely rescued by pro-angiogenic therapies. In humans, the placenta in late gestation secretes VEGF inhibitors like soluble FLT1 (sFLT1), and this is accentuated by multiple gestation and pre-eclampsia. This anti-angiogenic environment is accompanied by subclinical cardiac dysfunction, the extent of which correlates with circulating levels of sFLT1. Exogenous sFLT1 alone caused diastolic dysfunction in wild-type mice, and profound systolic dysfunction in mice lacking cardiac PGC-1α. Finally, plasma samples from women with PPCM contained abnormally high levels of sFLT1. These data indicate that PPCM is mainly a vascular disease, caused by excess anti-angiogenic signalling in the peripartum period. The data also explain how late pregnancy poses a threat to cardiac homeostasis, and why pre-eclampsia and multiple gestation are important risk factors for the development of PPCM.     

Reversal of pathological pain through specific spinal GABAA receptor subtypes

Inflammatory diseases and neuropathic insults are frequently accompanied by severe and debilitating pain, which can become chronic and often unresponsive to conventional analgesic treatment. A loss of synaptic inhibition in the spinal dorsal horn is considered to contribute significantly to this pain pathology. Facilitation of spinal gamma-aminobutyric acid (GABA)ergic neurotransmission through modulation of GABA(A) receptors should be able to compensate for this loss. With the use of GABA(A)-receptor point-mutated knock-in mice in which specific GABA(A) receptor subtypes have been selectively rendered insensitive to benzodiazepine-site ligands, we show here that pronounced analgesia can be achieved by specifically targeting spinal GABA(A) receptors containing the alpha2 and/or alpha3 subunits. We show that their selective activation by the non-sedative ('alpha1-sparing') benzodiazepine-site ligand L-838,417 (ref. 13) is highly effective against inflammatory and neuropathic pain yet devoid of unwanted sedation, motor impairment and tolerance development. L-838,417 not only diminished the nociceptive input to the brain but also reduced the activity of brain areas related to the associative-emotional components of pain, as shown by functional magnetic resonance imaging in rats. These results provide a rational basis for the development of subtype-selective GABAergic drugs for the treatment of chronic pain, which is often refractory to classical analgesics.     

Evidence for cooperative interactions in potassium channel gating.

Cloning and expression of voltage-activated potassium ion-channel complementary DNAs has confirmed that these channels are composed of four identical subunits, each containing a voltage sensor. It has been generally accepted that the voltage sensors must reach a permissive state through one or more conformational ('gating') transitions before the channel can open. To test whether each subunit gates independently, we have constructed cDNAs encoding four subunits on a single polypeptide chain, enabling us to specify the subunit stoichiometry. The gating of heterotetramers made up from combinations of subunits with different gating phenotypes strongly suggests that individual subunits gate cooperatively, rather than independently. Nonindependent subunit gating is consistent with measurements of the kinetics of K(+)-channel gating currents and in line with the widespread subunit cooperativity observed in other multisubunit proteins.     

Nitrogenase activity in a transfilter culture of rhizobia with a non-leguminous plant callus culture: Transfer of fixed15N2 from bacteria toPortulaca callus

Summary A transfilter culture of the non-leguminous plantPortulaca grandiflora var. JR andRhizobium sp. cowpea 32H1 was established. Using¹⁵N₂-analysis we demonstrated that¹⁵N-containing substances produced by the bacteria passed through the membrane and¹⁵N was enriched in the plant cells.Acknowledgment. The authors wish to express their gratitude to Prof. H. Marschner and Dr G. Hentschel for the determination of the nitrogen-content of our samples by the Dumasmethod and for advice on the optic emission method. Drs J. Burton, Milwaukee, Wisc., and Tjepkema, Oregon State University, are thanked for generous gifts ofRhizobium sp. cowpea 32H1. This work was supported by the DFG.