The second polar lobe of theSabellaria cementarium embryo plays an inhibitory role in apical tuft formation

Summary The embryo ofSabellaria cementarium (Polychaeta) forms a polar lobe at each of the first two cleavage divisions which becomes absorbed into one of the blastomeres at the end of the division. Lobe removal experiments show that the polar lobe preceding first cleavage is necessary for the development of the apical tuft and the posttrochal region of the trochophore larva. The polar lobe preceding second cleavage is smaller than the first polar lobe and is necessary only for post-trochal region development. In blastomere isolation experiments, isolates containing the C but not the D blastomere form apical tufts. Isolates containing the D but not the C blastomere do not form apical tufts. When the polar lobe preceding second cleavage is removed and the C and D blastomeres are separated and raised in isolation, each can form an apical tuft. When the second cleavage is equalized with sodium dodecyl sulfate (SDS) such that both the C and the D blastomeres receive second polar lobe material, no apical tuft is formed. These results suggest that apical tuft determinants are distributed to both the C and D blastomeres at second cleavage but that the second polar lobe contains an inhibitor for apical tuft formation which is shunted to the D blastomere after the completion of second cleavage.     

Effects of water conductivity on electrocommunication in the weak-electric fish Brienomyrus niger (Mormyriformes)

A characteristic electric organ discharge display in social encounters between mormyrid fish is a temporary discharge cessation. Using this response, we have investigated the useful range of electrocommunication under different water conductivity conditions in the mormyrid Brienomyrus niger. An individual fish was confined to a porous ceramic shelter tube and moved from a starting distance of 380 cm toward a similarly confined conspecific until discharge, cessation occurred. The moved fish was subsequently returned to its original, position. Water conductivity affects the peak-to-peak source voltage of the electric organ and the sensitivity of the fish's electroreceptors. Within a range of 10 to 36 000 μS/cm, the peak-to-peak amplitude of the electric organ discharge declined as a power function. At 120 μS/cm, the amplitude was 50%, and at 300μS/cm, 30% of the 10 μS/cm value. The interfish distance at which discharge cessation occurred and the associated electric field gradients were dependent on water conductivity and upon the spatial orientation of the two fish (end-to-end or parallel orientations of their shelter tubes). The respective ranges were from 135 cm and 0.02 mV/cm at 52 μS/cm (parallel orientation) to 22 cm and 0.36 mV/cm at 678 μS/cm (end-to-end orientation). When the data for both tube orientations were combined, the relationship between water conductivity (x) and the distance at which discharge cessation occurred (y) could be expressed by a power function, y=K·x^a (with K=10^2.97 and a=?0.56). When an electrically ‘silent’ fish was moved away from its conspecific, a discharge resumption in the form of a high-frequency rebound occasionally effected changes in the other fish's discharge activity at distances up to 157 cm (with an associated electric, field gradient of 0.01 mV/cm under the lowest conductivity condition).     

The identification of dimethylphenylarsine as a microbial metabolite using a simple method of chemofocusing

Candida humicola acts on benzenearsonic acid to produce dimethylphenylarsine, which was identified by mass spectroscopy following the chemofocusing of the volatile metabolite onto a mercuric chloride impregnated filter. The same technique established that trimethylarsine is the volatile metabolic product obtained from C. humicola treated with 4-NH₂-2-OHC₆H₃AsO(OH)₂ and (CH₃)₃AsO. Arsanilic acid, 4-NH₂C₆H₄AsO(OH)₂, is not metabolized to a volatile arsine.     

Heterochromatin accumulation,disposition and diversity in Gibasis karwinskyana (Commelinaceae)

C-banding differences within Gibasis karwinskyana (Roem & Schult.) Rohw. were reassessed using dual fluorochrome staining. Pronounced differences in C-band pattern between two subspecies with identical basic karyotypes were due to different chromosomal locations of AT-rich and GC-rich heterochromatin. The AT-rich component had an equilocal distribution in the karyotype and has evidently been accumulated at telomeres, as shown by its prevalence in supernumerary segments and B chromosomes. The GC-rich component also varied in amount, but was limited to nucleolus organizing regions (NORs) and centromeres. Centromeres and telomeres are suggested to constitute separate, although perhaps interdependent, centres of heterochromatin amplification. The possible role of nuclear architecture in determining the accumulation, distribution and spread of these sequences is discussed.Abbreviations H Hoechst 33258 - CMA chromomycin A3 - NOR nucleolus organizing region - SS supernumerary segment - Q quinacrine dihydrochloride - H⁺ H etc. indicate enhanced (+) and quenched (-) fluorescence with the stated fluorochrome by H.C. Macgregor     

Inhibitors of Urokinase and Thrombin in Cultured Neural Cells

Recent studies have suggested important roles for certain proteases and protease inhibitors in the growth and development of the CNS. In the present studies, inhibitors of urokinase or thrombin in cultured neural cells and serum-free medium from the cells were identified by screening for components that formed sodium dodecyl sulfate-stable complexes with 125I-urokinase or 125I-thrombin. Rinsed glioblastoma possessed two components that complexed 125I-urokinase. One was type 1 plasminogen activator inhibitor (PAI-1), because the 125I-urokinase-containing complexes were immunoprecipitated with anti-PAI-1 antibodies. The other component formed complexes with 125I-urokinase that were not recognized by antibodies to PAI-1 or protease nexin-1 (PN-1). Its identity is unknown. In addition to these cell-bound components, the glioblastoma cells also secreted two inhibitors that formed complexes with 125I-urokinase; one was PAI-1, and the other was PN-1. The secreted PN-1 also formed complexes with 125I-thrombin. It was the only thrombin inhibitor detected in these studies. Human neuroblastoma cells did not contain components that formed detectable complexes with either 125I-urokinase or 125I-thrombin. However, human neuroblastoma cells did contain very low levels of PN-1 mRNA and PN-1 protein. Added PN-1 bound to the surface of both glioblastoma and neuroblastoma cells. This interaction accelerated the inhibition of thrombin by PN-1 and blocked the ability of PN-1 to form complexes with 125I-urokinase. Thus, cell-bound PN-1 was a specific thrombin inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)     

Resolution of Biphasic Binding of the Opioid Antagonist Naltrexone in Brain Membranes

In synaptosomal membranes from rat brain cortex, in the presence of 150 mM NaCl, the opioid antagonist [3H]naltrexone bound to two populations of receptor sites with affinities of 0.27 and 4.3 nM, respectively. Guanosine-5'-(3-thiotriphosphate) had little modulating effect and did not alter the biphasic nature of ligand binding. On the other hand, receptor-selective opioids differentially inhibited the two binding components of [3H]naltrexone. As shown by nonlinear least-squares analysis, the mu opioids Tyr-D-Ala-Gly-(Me)Phe-Gly-ol or sufentanil abolished high-affinity [3H]naltrexone binding, whereas the delta-selective ligands [D-Pen2,D-Pen5]enkephalin, ICI 174,864, and oxymorphindole inhibited and eventually eliminated the low-affinity component in a concentration-dependent manner. These results indicate that, in contrast to the guanine nucleotide-sensitive biphasic binding of opioid-alkaloid agonists, the heterogeneity of naltrexone binding in brain membranes reflects ligand interaction with different opioid-receptor types.     

Sustained effects of biofeedback-assisted relaxation therapy in essential hypertension

The usefulness of biofeedback-assisted relaxation as an adjunct or substitute for pharmacotherapy in essential hypertension can be enhanced if the effects are shown to persist after formal treatment has ended. Patients with essential hypertension successfully treated with biofeedback-assisted relaxation were recalled for follow-up yearly after the termination of treatment. Twenty-six of 40 patients met the BP criterion for success. At one-, two-, and three-year follow-up, 31%, 38%, and 27% of the successful completers continued to meet the criterion for success. The pretreatment-posttreatment decreases in BP were accompanied by decreases in forehead muscle tension and urinary cortisol. Forehead muscle tension, urinary cortisol, and anxiety levels were significantly lower than pretreatment one year after the end of treatment. Self-report data were used to assess continued relaxation practice. No relationship was found between practice and any other dependent measure. It appears that some patients trained in biofeedback-assisted relaxation can maintain lowered blood pressure, muscle tension, anxiety, and cortisol levels over the long term; however, the role of relaxation practice in maintaining these lowered levels remains unclear.     

Specific reduction of delta-opioid receptor binding in transfected NG108-15 cells.

We have recently identified and sequenced the cDNA for an opioid-binding protein with homologies to cell adhesion molecules (OBCAM) (Schofield, P. R., McFarlard, K. C., Hayflick, J. S., Wilcox, J. N., Cho, T. M., Roy, S., Lee, N. M., Loh, H. H., and Seeburg, P. H. (1989) EMBO J. 8, 489-495). Several lines of evidence using antibodies suggest that OBCAM may play a functional role in NG108-15 neuroblastoma x glioma cells, a useful model system that contains a homogeneous population of delta-opioid receptors. A logical extension of this research is to further test this hypothesis. As part of this study, NG108-15 cells were stably transfected with either sense or antisense sequences of a portion of pROM, the rat cDNA for OBCAM. [3H] Diprenorphine binding was greatly reduced in antisense-transfected cells relative to non-transfected cells. Binding to alpha 2-adrenergic, muscarinic, and insulin receptors was unaffected. These results further support the notion that OBCAM or its analogue is part (or a subunit) of an opioid receptor. Furthermore, our observation of an apparently specific reduction in opioid binding in these transfected cells suggests that they may provide a novel genetic approach for studying regulation of the opioid receptor in this defined cell line.