Iridoid glucosides in fouquieriaceae

From three Fouquieria sp. 12 iridoid glucosides were isolated and identified. Eight of these were structurally related to galioside (monotropein methylester), while four were hydroxy substitution products of deoxyloganin. In three cases the glucoside occurred together with the corresponding 10-O-acetate.     

Can membrane excitation be described without a membrane capacity?

A simplified model of excitation is introduced in which the membrane capacity is ignored. It is shown that: (1) Threshold, action potentials, and strength-duration relation can be reproduced by a membrane without a capacity, even for a very simplified model. (2) The delayed build up of the sodium conductance can mimic a membrane capacity. (3) A constant potential stimulus can be used to reveal the influence of the membrane capacity, eventually combined with a feed back mechanism which reduces the effect of the capacity. (4) The effect of the membrane capacity depends on the ratio between the membrane time constant and the time constant for the fast conductance changes.     

Mucosal epithelial cells and Langerhans cells are targets for infection by the immunosuppressive type D retrovirus simian AIDS retrovirus serotype 1

Simian acquired immune deficiency syndrome (SAIDS) caused by the type D retrovirus SRV-1 results in opportunistic infections and a spectrum of oral lesions similar to those seen in humans with AIDS. To better understand the pathogenesis of these oral lesions we have retrospectively examined the oral mucosa from ten rhesus monkeys that died with SAIDS and prospectively examined the oral mucosa of ten additional animals inoculated with SRV-1 to determine at what time, and in what cells SRV-1 infection of the oral mucosa occurs. Using single and double label immunohistologic techniques, and electron microscopy we detected SRV-1 in clusters of oral epithelial cells and rare Langerhans cells as early as 1 month postinoculation.     

Phosphorylation of glycogen synthase I from human polymorphonuclear leukocytes

Summary Glycogen synthase I from human polymorphonuclear leukocytes was phosphorylated with cAMP dependent protein kinase, synthase kinase or phosvitin kinase prepared from these cells. Limited tryptic hydrolysis released four phosphopeptides (t-A, t-B, t-C, t-D). Subsequent α-chymotryptic hydrolysis of the trypsin resistant core released three phosphopeptides. (c-A, c-B, c-C). The kinetic changes of glycogen synthase were compared with the phosphorylation of the peptides. Equivalent kinetic changes (K_c=0.2–0.3 mM Glc-6-P) were obtained when 1 P_i/subunit was introduced by cAMP dependent protein kinase, 0.5 P_i/subunit by synthase kinase and 0.8 P_i/subunit by both kinases. Initially, cAMP dependent protein kinase phosphorylated peptides c-A and t-C in parallel and somewhat later also t-B, whereas synthase kinase initially phosphorylated only c-A. The ultimate effect of the two kinases on c-A was additive. It was concluded that the initial kinetic changes were dependent on phosphorylation of c-A, which contained two sites, one for each kinase. The same kinetic changes were induced by phosphorylation on each of the sites. In the subsequent phosphorylation the kinases, separately or together, phosphorylated peptide c-C indicating one non-specific phosphorylatable site in this peptide. The cAMP dependent protein kinase alone phosphorylated t-C maximally, whereas both kinases were required for an equal phosphorylation of t-A and t-B. It is suggested that the cAMP dependent protein kinase phosphorylated t-A and t-C, whereas the data did not allow a similar suggestion for t-B. The kinetic changes occurring during the later stages of phosphorylation were an increase in K_c for Glc. 6-P to 4–5 mM at 1.85 P_i/subunit and to 20 mM at 3.3 P_i/subunit, but the changes could not be assigned to phosphorylation of any specific peptide. Phosphorylation of the peptides t-D and c-B were insignificant, but c-B may be phosphorylated under other experimental conditions (25). The phosvitin kinase phosphorylated glycogen synthase extremely slowly to an extent of 0.8 P_i/subunit, mainly in peptide c-C. Glycogen synthase would appear without physiological importance as substrate for this kinase. Phosphorylase kinase from rabbit skeletal muscle incorporated 0.7 P_i/subunit, mainly in peptide c-A causing a decrease in RI to 0.3, which upon further incubation remained constant. The rate of decrease in RI to 0.5 was unaffected by several synthase modifiers, including Glc-6-P, but was inhibited by ADP and P_i. The rate of phosphorylation by cAMP dependent protein kinase and synthase kinase was diversely affected in different buffers, however, without affecting the ultimate phosphorylation pattern.     

Phosphorylation of glycogen synthase in a homogenate of human polymorphonuclear leukocytes

Summary Glycogen synthase I in a homogenate of human polymorphonuclear leukocytes was phosphorylated under imitated physiological conditions utilizing the endogenous protein kinases. At subsequent steps of phosphorylation the³²P-labelled synthase was purified and characterized. Limited tryptic hydrolysis of the³²P-labelled synthase released four phosphopeptides (t-A, t-B, t-C, t-D) and subsequent chymotrypsinization of the trypsin resistant core released three phosphopeptides (c-A, c-B, c-C). One P_i/subunit was incorporated within 8–10 min and 2.2 P_i/subunit within 60 min increasing the K_c for Gle-6-P to 4–6 mM. The initial phosphorylation up to 0.8 P_i/subunit occurred mainly in peptide c-A and a linear relation between ratio of independence (RI) of glycogen synthase in the interval RI 0.85 to RI 0.05 and phosphorylation of this peptide to 0.5 P_i was observed. Phosphorylation of this peptide is responsible for the decrease in ratio of independence. From experiments with inhibitors and activators, the initial phosphorylation was found predominantly catalysed by the endogenous cAMP independent synthase kinase, however, the endogenous cAMP dependent protein kinase and phosphorylase kinase also phosphorylate endogenous glycogen synthase I to a minor degree. Circumstantial evidence for a Ca-dependent synthase kinase different from phosphorylase kinase is presented. The endogenous Gle-6-P dependent glycogen synthase occurring in a homogenate of leukocytes disrupted in the presence of NaF incorporated 1.07 P_i/subunit and K_c for Glc-6-P was increased from 6–8 mM to 20 mM. From the present and previous experiments [7] a total of 8 major phosphorylatable sites have been defined, one on each of the peptides t-A, t-B, t-C, c-B and c-C and two on peptide c-A, which in addition may contain a third site for phosphorylase kinase. Assuming identical subunits, only 13 out of 32 sites are thus covalently modified at maximum phosphorylation. The operational defined synthase R (K_c for Glc-6-P 0.5 mM) and D (K_c for Glc-6-P 2–8 mM) activities correspond to synthase with about 0.8 P_i and 1.8–2.3 P_i/subunit, respectively.     

Abiotic formation of particles from extracellular organic carbon released by phytoplankton

¹⁴C-labeled extracellular organic carbon (EOC) released by the phytoplankton in a Danish Estuary was shown immediately to form particles (>0.2m) when the products were added to a natural water sample. About 14%–20% of the added activity could be recovered as particles. Any bacterial assimilation of the extracellular products was thus masked. The abiotic origin of the particulate EOC was verified, and it was shown that the particle formation was due to some factors present in the estuarine water with a nominal diameter >0.2m. Precaution must be taken to avoid misinterpretations in studies concerning carbon flow from algae to bacteria.     

Screening for antimicrobial resistance genes and virulence factors via genome sequencing

Second-generation genome sequencing and alignment of the resulting reads to in silico genomes containing antimicrobial resistance and virulence factor genes were used to screen for undesirable genes in 28 strains which could be used in human nutrition. No virulence factor genes were detected, while several isolates contained antimicrobial resistance genes.