New records of the River Shark Glyphis (Carcharhinidae) reported from Cape York Peninsula, northern Australia

The distribution of the river shark Glyphis in northern Australia is extended with new records of occurrence in the Gulf of Carpentaria and a reassessment of historical survey data from Cape York Peninsula. Nine new specimens of Glyphis sp. A were collected in 2005 from the Weipa region on the Queensland coast of the Gulf of Carpentaria. A re-examination of archival records from 1978-86 marine and estuarine fish surveys in the Gulf of Carpentaria and along the northern Queensland East Coast allowed a further nineteen Glyphis specimens to be identified. Combined this gives twenty-eight new records of Glyphis specimens from the coasts of Cape York Peninsula, Queensland. Common habitat characteristics for all captures were turbid, shallow, fast running tidal water in the upper reaches of coastal rivers. The substrate was generally muddy and the rivers lined with mangrove. In all surveys the representation of Glyphis was low, being less than 1% of the total shark captures historically and 0.002 sharks 50 m net hour-1 in Weipa 2005. The size range captured was 1000-1800 mm total length historically and 705-1200 mm total length from Weipa 2005, with none recorded as sexually mature. Diagnostic characteristics of the Weipa specimens, identified as Glyphis sp. A, were: lower jaw teeth protruding and "spear-like"; second dorsal fin greater than half the height of the first dorsal fin; the snout relatively short and fleshy in the lateral view; pectoral fin ventral surface black in colouration; the precaudal vertebral count between 118 and 123; and the total vertebral count between 204 and 209.

Annellosympodia orbiculata gen. et sp. nov. and Scolecostigmina flagellariae sp. nov. from Australia

Two new fungi, Annellosympodia orbiculata and Scolecostigmina flagellariae, on Acacia ligulata and Flagellaria indica, respectively, from Australia are described and illustrated. The former species is placed in the new genus Annellosympodia, which is characterised by an unusual combination of features, viz. fasciculate conidiogenous cells (conidiophores reduced to conidiogenous cells), holoblastic conidiogenesis with sympodial, but rectilinear proliferation leaving annular structures and lateral conspicuous conidiogenous loci, and rhexolytic conidial secession. The generic placement of these two fungi is discussed.

Smoking behaviour modifies IL23r-associated disease risk in patients with Crohn's disease

Background and Aim The etiology of Crohn's disease (CD) implicates both genetic and environmental factors. Smoking behavior is one environmental risk factor to play a role in the development of CD. The study aimed to assess the contribution of the interleukin 23 receptor (IL23R) in determining disease susceptibility in two independent cohorts of CD, and to investigate the interactions between IL23R variants, smoking behavior, and CD-associated genes, NOD2 and ATG16L1. Methods Ten IL23R single-nucleotide polymorphisms (SNPs) were genotyped in 675 CD cases, and 1255 controls from Brisbane, Australia (dataset 1). Six of these SNPs were genotyped in 318 CD cases and 533 controls from Canterbury, New Zealand (dataset 2). Case–control analysis of genotype and allele frequencies, and haplotype analysis for all SNPs was conducted. Results We demonstrate a strong increased CD risk for smokers in both datasets (odds ratio 3.77, 95% confidence interval 2.88–4.94), and an additive interaction between IL23R SNPs and cigarette smoking. Ileal involvement was a consistent marker of strong SNP–CD association (P ≤ 0.001), while the lowest minor allele frequencies for location were found in those with colonic CD (L2). Three haplotype blocks were identified across the 10 IL23R SNPs conferring different risk of CD. Haplotypes conferred no further risk of CD when compared with single SNP analyses. Conclusion IL23R gene variants determine CD susceptibility in the Australian and New Zealand population, particularly ileal CD. A strong additive interaction exists between IL23R SNPs and smoking behavior resulting in a dramatic increase in disease risk depending upon specific genetic background.