Anomalous carbonylation of [Pd(dppm)(O2CCF3)]2 to give an asymmetric μ-CO complex

The reactive palladium dimer, [Pd(dppm)(O₂CCF₃)]₂, is carbonylated to [Pd(dppm)(O₂CCF₃)]₂(μ-CO) in a reversible reaction with K = c. 7.2(2)x10⁴ atm⁻¹ (P_1/2 = c. 2.4 Torr). This is significantly larger than is expected based on the λ_max = 280 nm in the electronic spectrum. The product can be isolated in analytically pure form by crystallization under a CO atmosphere. It forms crystals in the monoclinic space group Cc with a = 18.584(5), b = 28.65(1), c = 11.164(3) Å and β = 95.16(2)°. The structure is significantly distorted. The bonding about the two palladium atoms is quite asymmetric. While one is close to a square planar geometry with a Pd---C(O) distance of 1.90(2) Å, the other is significantly pyramidalized and has a longer (2.00(2) Å) bond to the bridging CO. The Pd---Pd distance is only 2.896(2) Å, much shorter than that usually observed for formally non-bonded Pd atoms.     

Contrasting Neurochemical Interactions of Tiletamine, a Potent Phencyclidine (PCP) Receptor Ligand, with the N-Methyl-D-Aspartate-Coupled and -Uncoupled PCP Recognition Sites

Neurochemical interactions of tiletamine, a potent phencyclidine (PCP) receptor ligand, with the N-methyl-D-aspartate (NMDA)-coupled and -uncoupled PCP recognition sites were examined. Tiletamine potently displaced the binding of [3H]1-(2-thienyl)cyclohexylpiperidine with an IC50 of 79 nM without affecting sigma-, glycine, glutamate, kainate, quisqualate, or dopamine (DA) receptors. Like other PCP ligands acting via the NMDA-coupled PCP recognition sites, tiletamine decreased basal, harmaline-, and D-serine-mediated increases in cyclic cGMP levels and induced stereotypy and ataxia. Tiletamine was nearly five times more potent than PCP at inhibiting the binding of 3-hydroxy[3H]PCP to its high-affinity NMDA-uncoupled PCP recognition sites. However, following parenteral administration, dizocilpine maleate (MK-801), ketamine, PCP, dexoxadrol, and 1-(2-thienyl)cyclohexylpiperidine HCl, but not tiletamine, increased rat pyriform cortical DA metabolism and/or release, a response modulated by the NMDA-uncoupled PCP recognition sites. Pretreatment with tiletamine did not attenuate the MK-801-induced increases in rat pyriform cortical DA metabolism, a result suggesting that tiletamine is not a partial agonist of the NMDA-uncoupled PCP recognition sites in this region. However, following intracerebroventricular administration (100-500 micrograms/rat), tiletamine increased pyriform cortical DA metabolism with a bell-shaped dose-response curve. These data indicate a differential interaction of tiletamine with the NMDA-coupled and -uncoupled PCP recognition sites. The paradoxical effects of tiletamine suggest that tiletamine might activate receptor(s) or neuronal pathways of unknown pharmacology.     

Sodium-dependent nucleoside transport in choroid plexus from rabbit. Evidence for a single transporter for purine and pyrimidine nucleosides.

The overall goal of this study was to determine the mechanisms by which nucleosides are transported in choroid plexus. Choroid plexus tissue slices obtained from rabbit brain were depleted of ATP with 2,4-dinitrophenol. Uridine and thymidine accumulated in the slices against a concentration gradient in the presence of an inwardly directed Na+ gradient. The Na(+)-driven uptake of uridine and thymidine was saturable with Km values of 18.1 +/- 2.0 and 13.0 +/- 2.3 microM and Vmax values of 5.5 +/- 0.3 and 1.0 +/- 0.2 nmol/g/s, respectively. Na(+)-driven uridine uptake was inhibited by naturally occurring ribo- and deoxyribonucleosides (adenosine, cytidine, and thymidine) but not by synthetic nucleoside analogs (dideoxyadenosine, dideoxycytidine, cytidine arabinoside, and 3'-azidothymidine). Both purine (guanosine, inosine, formycin B) and pyrimidine nucleosides (uridine and cytidine) were potent inhibitors of Na(+)-thymidine transport with IC50 values ranging between 5 and 23 microM. Formycin B competitively inhibited Na(+)-thymidine uptake and thymidine trans-stimulated formycin B uptake. These data suggest that both purine and pyrimidine nucleosides are substrates of the same system. The stoichiometric coupling ratios between Na+ and the nucleosides, guanosine, uridine, and thymidine, were 1.87 +/- 0.10, 1.99 +/- 0.35, and 2.07 +/- 0.09, respectively. The system differs from Na(+)-nucleoside co-transport systems in other tissues which are generally selective for either purine or pyrimidine nucleosides and which have stoichiometric ratios of 1. This study represents the first direct demonstration of a unique Na(+)-nucleoside co-transport system in choroid plexus.     

Description of the oöcysts of three new species of coccidia (Apicomplexa: Eimeriidae) from lizards in Namibia

Three new species of coccidian were recovered from the intestinal contents and faeces of lizards in Namibia, southwest Africa. Oöcysts of Eimeria barnardi n. sp. are described from Rhoptropus barnardi (Gekkonidae) and are ellipsoidal, 24.3 × 19.9 (21–26.5 × 16–22) m; shape index (length/width) 1.22 (1.12–1.30). A micropyle and oöcyst residuum are absent but a fragmented polar granule is present. Sporocysts are subspherical, 9.2 × 8.3 (8–11 × 7.5–9) m; shape index 1.11 (1.02–1.27). Oöcysts of Eimeria pachybibroni n. sp. were found in Pachydactylus bibroni (Gekkonidae) and are ellipsoidal, 26.2 × 18.2 (21.5–28 × 16–19) m; shape index 1.44 (1.30–1.52). A micropyle and oöcyst residuum are absent but a polar granule is present. Sporocysts are subspherical, 8.9 × 8.0 (8–9.5 × 7–8.5) m; shape index 1.12 (1.03–1.20). Oöcysts of Isospora spilogaster n. sp. are reported from Mabuya spilogaster (Scincidae) and are subspherical, 27.4 × 26.0 (21.5–35 × 21–35) m; shape index 1.05 (1.00–1.13). Micropyle, oöcyst residuum and polar granules are absent. Sporocysts are ellipsoidal, 13.2 × 9.7 (10.5–15 × 9–11) m; shape index 1.36 (1.08–1.50).     

Description of the oöcysts of two new species of Eimeria (Apicomplexa: Eimeriidae) from the rough earth snake Virginia striatula (Serpentes: Colubridae) in Texas and Arkansas

Coccidian oöcysts recovered from the faeces of rough earth snakes Virginia striatula (Serpentes: Colubridae) were found to represent two previously unreported eimerians. Oöcysts of Eimeria desotoensis n. sp. were found in 5/32 (16%) of the snakes and were spherical to ellipsoidal, 18.4 × 17.2 (15–21.5 × 15–19.5) μm, with a thin, single-layered wall; their shape-index (length/width) was 1.07 (1.00–1.23). A micropyle and oöcyst residuum were absent; polar granule were present in 33% of the oöcysts. The sporocysts were ovoidal, 11.5 × 7.6 (10.5–13 × 7–8) μm, with a Stieda body; their shape-index was 1.51 (1.30–1.68). The sporocyst residuum was moderate in size and composed of a cluster of granules. Oöcysts of Eimeria hobartsmithi n. sp. were found in 2/32 (6%) of the snakes and were subspherical to ellipsoidal, 18.0 × 15.7 (16–20 × 15–17) μm, with a thin, single-layered wall; their shape-index was 1.15 (1.02–1.32). A micropyle, oöcyst residuum and polar granule were absent. The sporocysts were elongate, 13.2 × 6.3 (12–14.5 × 6–6.5) μm, with a Stieda body; their shape-index was 2.10 (1.88–2.34). A large sporocyst residuum was present in each sporocyst, often obscuring the sporozoites. In addition to the two new species, oöcysts of E. striatula Upton & McAllister, 1990 were observed in 38% of the snakes.     

Pearson syndrome and mitochondrial encephalomyopathy in a patient with a deletion of mtDNA.

A patient is described who has features of Pearson syndrome and who presented in the neonatal period with a hypoplastic anemia. He later developed hepatic, renal, and exocrine pancreatic dysfunction. At the age of 5 years he developed visual impairment, tremor, ataxia, proximal muscle weakness, external ophthalmoplegia, and a pigmentary retinopathy (Kearns-Sayre syndrome). Muscle biopsy confirmed the diagnosis of mitochondrial myopathy. Analysis of mtDNA from leukocytes and muscle showed mtDNA heteroplasmy in both tissues, with one population of mtDNA deleted by 4.9 kb. The deleted region was bridged by a 13-nucleotide sequence occurring as a direct repeat in normal mtDNA. Both Pearson syndrome and Kearns-Sayre syndrome have been noted to be associated with deletions of mtDNA; they have not previously been described in the same patient. These observations indicate that the two disorders have the same molecular basis; the different phenotypes are probably determined by the initial proportion of deleted mtDNAs and modified by selection against them in different tissues.