Recovery of Trichuris tenuis Chandler, 1930, from camelids (Lama glama and Vicugna vicugna) in Argentina

A survey of whipworms was conducted in llamas and vicu?as in northwestern Argentina. Fecal examinations of a group of 14 llamas (April 1995-March 1996) and 69 vicu?as (November 1996) indicated a high prevalence (usually >50%) of Trichuris sp. in these hosts. Prevalence was highest during July-November 1995 that also coincided with the highest mean fecal egg count. During postmortem examinations of 1 llama and 1 vicu?a, specimens of Trichuris tenuis were recovered from the cecum/large intestine of each camelid. This is the first report of T. tenuis in South America, and the first report in the vicu?a. It is suggested that T. tenuis is the typical whipworm of aboriginal camelids.     

The life cycle of Amblyomma neumanni Ribaga, 1902 (Acari: Ixodidae) in the laboratory

A colony of Amblyomma neumanni was started with engorged females collected from cattle in the province of Salta (24° 51S, 65° 33W), Argentina. The larvae and nymphs were fed on rabbits and the adults on calves. The non-parasitic stages were maintained in darkness at 27 ± 1°C and 83–86% RH. The life cycle (pre-feeding period not tested) had a mean duration of 205.7 days. The mean time (days) for the different phases of the cycle were as follows: feeding of females 8.8, pre-oviposition 23.8, oviposition 41.4, minimum egg incubation 76.1, feeding of larvae 8.5, pre-moult to nymphs 16.4, feeding of nymphs 7.9 and pre-moult to adults 22.8. The mean recovery rates of larvae, nymphs and females were 83.8, 85.6 and 89.3%, respectively. The nymphs moulting to females were heavier (8.1 ± 2.34 mg) than those moulting to males (6.0 ± 2.34 mg; p < 0.01), but their range of engorgement weight showed overlap (2.3–16.2 versus 2.2–12.8 mg, respectively). Two gynandromorphs were detected between the nymphs. A comparison of biological parameters of A. neumanni with other American Amblyomma species from mammals is presented. © Rapid Science Ltd. 1998     

Coralline algae indicate Pleistocene evolution from deep,open platform to outer barrier reef environments in the northern Great Barrier Reef margin

Coralline algae from a drill core in Ribbon Reef 5 have been used to interpret changes in the depositional palaeoenvironments in the northern Australian Great Barrier Reef over the last 790 ka. Three main coralline algal assemblages, each dominated by members of a particular subfamily, have been distinguished by quantitative analysis: (1) mastophoroid assemblages, usually occurring as crusts on corals, are typical of the shallowest reef settings; (2) lithophylloid assemblages within algal nodules may represent shallow-water, cooler environments or deeper reef subenvironments; and (3) melobesioid assemblages are characteristic of deeper-water platform areas. The algal assemblages between 96 and 210 m b.s.f. (metre below sea floor) record a fluctuating but progressive shallowing-upwards from deep, outer-platform to shallower, non-reefal depositional environments. Two intervening episodes dominated by mastophoroids represent two phases of reef growth. The section above 96 m b.s.f. comprises several stacked reefs in which mastophoroid crusts similar to the present-day shallow-water assemblages predominate.Electronic Supplementary Material Supplementary material is available for this article at .Communicated by: Geological Editor P.K. Swart     

Validation of the Diagnostic Interview for Genetic Studies (DIGS) in Colombia

An interview tool, Diagnostic Interview for Genetic Studies (DIGS 3.0), was translated into Spanish for application in studies of psychiatric disorders in Colombia. Two Spanish translations of the original English version of DIGS were prepared and back-translated into English. A review committee verified the linguistic and cultural equivalence of the translations. The evaluator and test-retest reliability were assessed calculating Cohen's kappa for samples of 65 and 91 patients respectively. DIGS proved valid in both appearance and content. The confidence interval (C.I.) was excellent for schizophrenia (kappa = 0.81, C.I. 95% = 0.68-0.93), bipolar disorder (kappa = 0.87, C.I. 95% = 0.75-0.99), major depressive disorder (kappa = 0.86, C.I. 95% = 0.70-1.00), and for a normal diagnosis (kappa = 0.65, C.I. 95% = 0.41-0.89); it was good for other psychiatric diagnosis (kappa = 0.65, C.I. 95% = 0.41-0.89) and poor for schizoaffective disorder (kappa = 0.37, C.I. 95% = -0.02-0.76). Test-retest reliability was excellent for all diagnoses (kappa > 0.8), except for "other psychiatric diagnoses" (kappa = 0.64, C.I. 95% = 0.31-0.96). The Spanish translation of the DIGS was comprehensible, with face and content validity, and good test-retest and evaluator reliability. This translation will be a useful tool for genetic studies of psychiatric disorders in Latin America, particularly where schizophrenia and affective disorders are involved.     

The -308 polymorphism in the promoter region of the tumor necrosis factor-alpha (TNF-alpha) gene and ex vivo lipopolysaccharide-induced TNF-alpha expression in patients with aggressive periodontitis and/or type 1 diabetes mellitus

Several single-nucleotide polymorphisms (SNPs) have been identified in the TNF-alpha gene promoter. The transition G-->A at position -308 generates the TNF-alpha1 (G/G) and TNF-alpha2 (G/A or A/A) alleles, where the polymorphic TNF-alpha2 allele is associated with a high, in vitro TNF-alpha expression and an increased susceptibility to diverse illnesses. Here we study the association of the -308 TNF-alpha SNP with the susceptibility for developing aggressive periodontitis (AP), AP combined with type 1 diabetes mellitus (DM) and DM. We also explore the TNF-alpha capability expression and the presence of the -308 polymorphism. For this purpose we recruited 27 individuals with AP (AP+ group), 27 individuals with AP combined with DM (AP+/DM+ group), and 27 individuals with DM without signs of periodontitis upon clinical examination (DM+ group). The control group was comprised of 30 subjects. Genotyping for TNF-alpha promoter was performed by PCR-RFLP analysis. For TNF-alpha expression we used a blood culture system.     

Iron porphyrin treatment extends survival in a transgenic animal model of amyotrophic lateral sclerosis

Oxidative damage, produced by mutant Cu/Zn superoxide dismutase (SOD1), may play a role in the pathogenesis of amyotrophic lateral sclerosis (ALS), a devastating motor neuron degenerative disease. A novel approach to antioxidant therapy is the use of metalloporphyrins that catalytically scavenge a wide range of reactive oxygen and reactive nitrogen species. In this study, we examined the therapeutic potential of iron porphyrin (FeTCPP) in the G93A mutant SOD1 transgenic mouse model of ALS. We found that intraperitoneal injection of FeTCPP significantly improved motor function and extended survival in G93A mice. Similar results were seen with a second group of mice wherein treatment with FeTCPP was initiated at the onset of hindlimb weakness-roughly equivalent to the time at which treatment would begin in human patients. FeTCPP-treated mice also showed a significant reduction in levels of malondialdehyde (a marker of lipid peroxidation), in total content of protein carbonyls (a marker of protein oxidation), and increased neuronal survival in the spinal cord. These results therefore provide further evidence of oxidative damage in a mouse model of ALS, and suggest that FeTCPP could be beneficial for the treatment of ALS patients.     

SakA MAP kinase is involved in stress signal transduction,sexual development and spore viability in Aspergillus nidulans

In eukaryotic cells, environmental stress signals are transmitted by evolutionarily conserved MAPKs, such as Hog1 in the budding yeast Saccharomyces cerevisiae, Spc1 in the fission yeast Schizosaccharomyces pombe and p38/JNK in mammalian cells. Here, we report the identification of the Aspergillus nidulans sakA gene, which encodes a member of the stress MAPK family. The sakA gene is able to complement the S. pombe spc1- defects in both osmo-regulation and cell cycle progression. Moreover, SakA MAPK is activated in response to osmotic and oxidative stress in both S. pombe and A. nidulans. However, in contrast to hog1 and spc1 mutants, the sakA null mutant is not sensitive to high osmolarity stress, indicating a different regulation of the osmostress response in this fungus. On the other hand, the DeltasakA mutant shows development and cell-specific phenotypes. First, it displays premature steA-dependent sexual development. Second, DeltasakA mutant produces asexual spores that are highly sensitive to oxidative and heat shock stress and lose viability upon storage. Indeed, SakA is transiently activated early after induction of conidiation. Our results indicate that SakA MAPK is involved in stress signal transduction and repression of sexual development, and is required for spore stress resistance and survival.     

Linkage mapping of the primary disease locus for collie eye anomaly

Collie eye anomaly (cea) is a hereditary ocular disorder affecting development of the choroid and sclera segregating in several breeds of dog, including rough, smooth, and Border collies and Australian shepherds. The disease is reminiscent of the choroidal hypoplasia phenotype observed in humans in conjunction with craniofacial or renal abnormalities. In dogs, however, the clinical phenotype can vary significantly; many dogs exhibit no obvious clinical consequences and retain apparently normal vision throughout life, while severely affected animals develop secondary retinal detachment, intraocular hemorrhage, and blindness. We report genetic studies establishing that the primary cea phenotype, choroidal hypoplasia, segregates as an autosomal recessive trait with nearly 100% penetrance. We further report linkage mapping of the primary cea locus to a 3.9-cM region of canine chromosome 37 (LOD = 22.17 at theta = 0.076), in a region corresponding to human chromosome 2q35. These results suggest the presence of a developmental regulatory gene important in ocular embryogenesis, with potential implications for other disorders of ocular vascularization.