Redescription of Retilaskeya horrida (di Monterosato, 1874) comb. nov. and a re-evaluation of the taxonomic affinity of the genus Retilaskeya (Caenogastropoda: Triphoroidea)

The family Cerithiopsidae H. Adams and A. Adams, 1853 is distributed worldwide, and comprises around 800 extant species divided into ~40 genera. The most speciose genus within the family is Cerithiopsis Forbes and Hanley, 1850, a taxon currently used as a general receptacle rather than as a proper phylogenetic lineage. We hereby redescribe the rare species Cerithiopsis horrida di Monterosato, 1874, review its nomenclature, known material, and distribution as well as figure the entire protoconch, operculum, and radula for the first time. Our results highlight extreme differences between ‘Cerithiopsis’ horrida and the Cerithiopsis type species Cerithiopsis tubercularis (Montagu, 1803) and strong morphological and radular similarities with species belonging to the genus Retilaskeya Marshall, 1978. A wide discussion lists several taxa that might be ascribed to the same group of species, which presumably constitute a different worldwide lineage. Pending relevant molecular phylogenetic studies of the Triphoroidea Gray, 1847, for morphological conformity we suggest transferring ‘Cerithiopsis’ horrida to the genus Retilaskeya, and the same action is presumably appropriate for its possible sister species ‘Cerithiopsis’ leopardus Rolán and Gori, 2013. Finally, Retilaskeya better conforms to Newtoniellidae Korobkov, 1955 than Cerithiopsidae.     

Hormonal control of Mg2+ transport in the heart

Magnesium is abundant in the mammalian body and the second most abundant cation in cells. Because the concentration of intracellular free Mg2+ is relatively high (0.2-1 mM), Mg2+ is unlikely to act as a second messenger, like Ca2+, by rapidly changing its cytosolic concentration. But changes in Mg2+ do have profound effects on cellular metabolism, structure and bioenergetics. Key enzymes or metabolic pathways, mitochondrial ion transport, Ca2+ channel activities in the plasma membrane and intracellular organelles, ATP-requiring reactions, and structural properties of cells and nucleic acids are modified by changes in Mg2+ concentration. Yet, although some information is available from giant cells and bacteria, little is known about the regulation of intracellular Mg2+ in mammalian cells. Here we report a new transport mechanism for Mg2+ across the sarcolemma of cardiac cells in both intact hearts and dissociated myocytes. We show that noradrenaline, through beta-adrenergic stimulation and increase of cyclic AMP, stimulates a large efflux of Mg2+ from cardiac cells. This transport is of major dimensions and can move up to 20% of total cellular Mg2+ within a few minutes.     

Defective tryptophan catabolism underlies inflammation in mouse chronic granulomatous disease

Half a century ago, chronic granulomatous disease (CGD) was first described as a disease fatally affecting the ability of children to survive infections. Various milestone discoveries have since been made, from an insufficient ability of patients' leucocytes to kill microbes to the underlying genetic abnormalities. In this inherited disorder, phagocytes lack NADPH oxidase activity and do not generate reactive oxygen species, most notably superoxide anion, causing recurrent bacterial and fungal infections. Patients with CGD also suffer from chronic inflammatory conditions, most prominently granuloma formation in hollow viscera. The precise mechanisms of the increased microbial pathogenicity have been unclear, and more so the reasons for the exaggerated inflammatory response. Here we show that a superoxide-dependent step in tryptophan metabolism along the kynurenine pathway is blocked in CGD mice with lethal pulmonary aspergillosis, leading to unrestrained Vgamma1(+) gammadelta T-cell reactivity, dominant production of interleukin (IL)-17, defective regulatory T-cell activity and acute inflammatory lung injury. Although beneficial effects are induced by IL-17 neutralization or gammadelta T-cell contraction, complete cure and reversal of the hyperinflammatory phenotype are achieved by replacement therapy with a natural kynurenine distal to the blockade in the pathway. Effective therapy, which includes co-administration of recombinant interferon-gamma (IFN-gamma), restores production of downstream immunoactive metabolites and enables the emergence of regulatory Vgamma4(+) gammadelta and Foxp3(+) alphabeta T cells. Therefore, paradoxically, the lack of reactive oxygen species contributes to the hyperinflammatory phenotype associated with NADPH oxidase deficiencies, through a dysfunctional kynurenine pathway of tryptophan catabolism. Yet, this condition can be reverted by reactivating the pathway downstream of the superoxide-dependent step.     

Non-redundant role of the long pentraxin PTX3 in anti-fungal innate immune response

Pentraxins are a superfamily of conserved proteins that are characterized by a cyclic multimeric structure. The classical short pentraxins, C-reactive protein (CRP) and serum amyloid P component (SAP), are acute-phase proteins produced in the liver in response to inflammatory mediators. Short pentraxins regulate innate resistance to microbes and the scavenging of cellular debris and extracellular matrix components. In contrast, long pentraxins have an unrelated, long amino-terminal domain coupled to the carboxy-terminal pentraxin domain, and differ, with respect to short pentraxins, in their gene organization, chromosomal localization, cellular source, and in their stimuli-inducing and ligand-recognition ability. To investigate the in vivo function of the long pentraxin PTX3, we generated mice deficient in Ptx3 by homologous recombination. Ptx3-null mice were susceptible to invasive pulmonary aspergillosis. Ptx3 binds selected microbial agents, including conidia of Aspergillus fumigatus, and we found that susceptibility of Ptx3-null mice was associated with defective recognition of conidia by alveolar macrophages and dendritic cells, as well as inappropriate induction of an adaptive type 2 response. Thus, the long pentraxin Ptx3 is a secreted pattern-recognition receptor that has a non-redundant role in resistance to selected microbial agents, in particular to the opportunistic fungal pathogen Aspergillus fumigatus.     

An intense stratospheric jet on Jupiter

The Earth's equatorial stratosphere shows oscillations in which the east-west winds reverse direction and the temperatures change cyclically with a period of about two years. This phenomenon, called the quasi-biennial oscillation, also affects the dynamics of the mid- and high-latitude stratosphere and weather in the lower atmosphere. Ground-based observations have suggested that similar temperature oscillations (with a 4-5-yr cycle) occur on Jupiter, but these data suffer from poor vertical resolution and Jupiter's stratospheric wind velocities have not yet been determined. Here we report maps of temperatures and winds with high spatial resolution, obtained from spacecraft measurements of infrared spectra of Jupiter's stratosphere. We find an intense, high-altitude equatorial jet with a speed of approximately 140 m s(-1), whose spatial structure resembles that of a quasi-quadrennial oscillation. Wave activity in the stratosphere also appears analogous to that occurring on Earth. A strong interaction between Jupiter and its plasma environment produces hot spots in its upper atmosphere and stratosphere near its poles, and the temperature maps define the penetration of the hot spots into the stratosphere.     

Chronic granulomatous disease

Chronic granulomatous disease is an inherited disorder of the NADPH oxidase characterized by severe bacterial and fungal infections and disordered inflammation. We propose that NADPH oxidase has a key role in regulating acute neutrophilic and T cell responses, which in turn restrains fungal growth and calibrates the inflammatory response to minimize injury and allergy. In this model, superoxide-induced activation of indoleamine 2,3-dioxygenase (IDO) is a central mechanism by which the optimal balance of antifungal host defense and immune tolerance occurs. This model is based on studies in mice and requires correlation in humans. Received 18 August 2008; received after revision 29 November 2008; accepted 16 December 2008