Malformed trilobites from the Cambrian, Ordovician, and Silurian of Australia.

Biomineralised remains of trilobites provide important insight into the evolutionary history of a diverse, extinct group of arthropods. Their exoskeletons are also ideal for recording malformations, including evidence of post-injury repair. Re-examination of historic collections and the study of new specimens is important for enhancing knowledge on trilobite malformations across this diverse clade.

Five new malformed trilobites from Cambrian and Ordovician deposits from the Natural History Museum.

Injured trilobites present insight into how a completely extinct group of arthropods responded to traumatic experiences, such as failed predation and moulting complications. These specimens are therefore important for more thoroughly understanding the Paleozoic predator-prey systems that involved trilobites. To expand the record of injured trilobites, we present new examples of injured and from the Campsite Cliff Shale Member of the Burgess Shale Formation (Cambrian, Miaolingian, Wuliuan), () from the Jince Formation (Cambrian, Miaolingian, Drumian), from the Llanfawr Mudstones Formation (Middle-Late Ordovician, Darriwilian-Sandbian), and from the Meadowtown Formation, (Middle-Late Ordovician, Darriwilian-Sandbian).

Examining abnormal Silurian trilobites from the Llandovery of Australia.

Abnormal trilobites present insight into how arthropods with fully biomineralised exoskeletons recovered from injuries, genetic malfunctions, and pathologies. Records of abnormal Silurian trilobites in particular show an abundance of specimens with teratologies and a limited record of injuries. Here we expand the record of abnormal Silurian trilobites by presenting seven new abnormal specimens of from the early Silurian (Llandovery, Telychian) Cotton Formation, New South Wales.

An earliest Triassic age for and comments on synchrotron tomography of Gondwanan horseshoe crabs.

Constraining the timing of morphological innovations within xiphosurid evolution is central for understanding when and how such a long-lived group exploited vacant ecological niches over the majority of the Phanerozoic. To expand the knowledge on the evolution of select xiphosurid forms, we reconsider the four Australian taxa: , and . In revisiting these taxa, we determine that, contrary to previous suggestion, arose after the Permian and the origin of over-developed genal spine structures within Austrolimulidae is exclusive to the Triassic.

A Lagerstätte from Australia provides insight into the nature of Miocene mesic ecosystems.

Reduced precipitation in the Miocene triggered the geographic contraction of rainforest ecosystems around the world. In Australia, this change was particularly pronounced; mesic rainforest ecosystems that once dominated the landscape transformed into the shrublands, grasslands, and deserts of today. A lack of well-preserved fossils has made it difficult to understand the nature of Australian ecosystems before the aridification.

Teratological trilobites from the Silurian (Wenlock and Ludlow) of Australia.

Documentation of malformed trilobites has presented invaluable insight into the palaeobiology of a wholly extinct euarthropod group. Although the northern hemisphere record is relatively well documented, examples of abnormal trilobites from Australia are limited. Furthermore, most recorded specimens are from Cambrian-aged rocks.

Trilobites and agnostids from the Goyder Formation (Cambrian Series 3, Guzhangian; Mindyallan), Amadeus Basin, central Australia.

A new assemblage containing twenty-two species of trilobites and agnostids is described from the Goyder Formation (Cambrian Series 3) in the Ross River Syncline and Gardiner Ranges of the Amadeus Basin, Northern Territory, central Australia. New trilobite taxa described include the genus, Trephina gen. nov.

Minor genomic differences between related B6 and B10 mice affect severity of schistosome infection by governing the mode of dendritic cell activation.

Infection with the helminth Schistosoma mansoni results in hepatointestinal granulomatous inflammation mediated by CD4 T cells directed against parasite eggs. The severity of disease varies greatly in humans and mice; however, the genetic basis of such a heterogenous immune response remains poorly understood. Here we show that, despite their close genetic relationship, C57BL/10SnJ (B10) mice developed significantly more pronounced immunopathology and higher T helper 17 cell responses than C57BL/6J (B6) mice.

Dysfunctional Cognitions among Offspring of Individuals with Bipolar Disorder.

Background: Individuals with bipolar disorder often endorse dysfunctional beliefs consistent with cognitive models of bipolar disorder (Beck, 1976; Mansell, 2007).

Aims: The present study sought to assess whether young adult offspring of those with bipolar disorder would also endorse these beliefs, independent of their own mood episode history.

Method: Participants (N = 89) were young adult college students with a parent with bipolar disorder (n = 27), major depressive disorder (MDD; n = 30), or no mood disorder (n = 32).

The microbial metabolites, short-chain fatty acids, regulate colonic Treg cell homeostasis.

Regulatory T cells (Tregs) that express the transcription factor Foxp3 are critical for regulating intestinal inflammation. Candidate microbe approaches have identified bacterial species and strain-specific molecules that can affect intestinal immune responses, including species that modulate Treg responses. Because neither all humans nor mice harbor the same bacterial strains, we posited that more prevalent factors exist that regulate the number and function of colonic Tregs.

Induction and regulation of pathogenic Th17 cell responses in schistosomiasis.

Schistosomiasis is a major tropical disease caused by trematode helminths in which the host mounts a pathogenic immune response against tissue-trapped parasite eggs. The immunopathology consists of egg antigen-specific CD4 T cell-mediated granulomatous inflammation that varies greatly in magnitude in humans and among mouse strains in an experimental model. New evidence, covered in this review, intimately ties the development of severe pathology to IL-17-producing CD4 T helper (Th17) cells, a finding that adds a new dimension to the traditional CD4 Th1 vs.

The pathogenic Th17 cell response to major schistosome egg antigen is sequentially dependent on IL-23 and IL-1β.

CBA/J mice infected with the helminth Schistosoma mansoni develop severe CD4 T cell-mediated hepatic granulomatous inflammation against parasite eggs associated with a robust Th17 cell response. We investigated the requisites for Th17 cell development using novel CD4 T cells expressing a transgenic TCR specific for the major Sm-p40 egg Ag, which produce IL-17 when stimulated with live schistosome eggs. Neutralization of IL-23 or blockade of the IL-1 receptor, but not IL-6 neutralization, abrogated egg-induced IL-17 secretion by transgenic T cells, whereas exogenous IL-23 or IL-1β reconstituted their ability to produce IL-17 when stimulated by syngeneic IL-12p40-deficient dendritic cells.

IRAK-2 regulates IL-1-mediated pathogenic Th17 cell development in helminthic infection.

Infection with the trematode parasite Schistosoma mansoni results in distinct heterogeneity of disease severity both in humans and in mice. In the experimental mouse model, severe disease is characterized by pronounced hepatic egg-induced granulomatous inflammation mediated by CD4 Th17 cells, whereas mild disease is associated with reduced hepatic inflammation in a Th2-skewed cytokine environment. Even though the host's genetic background significantly impacts the clinical outcome of schistosomiasis, specific gene(s) that contribute to disease severity remain elusive.

The gut microbiota and mucosal T cells.

It is intuitive that immune cells in the gut may require microbiota-derived cues for their differentiation. The proximity between host and microbe in the intestine would seemingly necessitate co-adaptation. However, it has been challenging to determine the members and features of the gut microbiota that influence immune system development and function.

T-bet protects against exacerbation of schistosome egg-induced immunopathology by regulating Th17-mediated inflammation.

C57BL/6 mice infected with Schistosoma mansoni naturally develop mild CD4(+) T-cell-mediated immunopathology characterized by small hepatic granulomas around parasite eggs. However, immunization with soluble egg Ag in CFA markedly exacerbates the lesions by inducing a potent proinflammatory environment with high levels of IFN-gamma and IL-17, which are signature cytokines of distinct Th1- versus Th17-cell lineages. To determine the relative role of these subsets in disease exacerbation, we examined mice deficient in T-bet (T-bet(-/-)), which is required for Th1 differentiation and IFN-gamma production.

Genetic control of severe egg-induced immunopathology and IL-17 production in murine schistosomiasis.

Infection with the trematode parasite Schistosoma mansoni results in a distinct heterogeneity of disease severity, both in humans and in an experimental mouse model. Severe disease is characterized by pronounced hepatic egg-induced granulomatous inflammation in a proinflammatory cytokine environment, whereas mild disease corresponds with reduced hepatic inflammation in a Th2 skewed cytokine environment. This marked heterogeneity indicates that genetic differences play a significant role in disease development, yet little is known about the genetic basis of dissimilar immunopathology.

Dendritic cell IL-23 and IL-1 production in response to schistosome eggs induces Th17 cells in a mouse strain prone to severe immunopathology.

Infection with schistosomes results in a CD4 T cell-mediated inflammatory reaction against parasite eggs that varies greatly in magnitude both in humans as well as in mice. In the murine disease, the severe form of immunopathology correlates with high levels of IL-17. We now report that live schistosome eggs stimulate dendritic cells from high pathology-prone CBA mice to produce IL-12p40, IL-6, and TGF-beta, whereas those from low pathology-prone BL/6 mice only make TGF-beta.

Coinfection with the intestinal nematode Heligmosomoides polygyrus markedly reduces hepatic egg-induced immunopathology and proinflammatory cytokines in mouse models of severe schistosomiasis.

Infection with the trematode helminth Schistosoma mansoni results in a parasite egg-induced, CD4 T-cell-mediated, hepatointestinal granulomatous and fibrosing inflammation that varies greatly in severity, with a higher frequency of milder forms typically occurring in regions where the disease is endemic. One possible explanation for this is that in these regions the degree of inflammation is lessened by widespread concurrent infection with gastrointestinal nematodes. We tested this hypothesis by establishing a murine coinfection model in which mice were infected with the intestinal nematode parasite Heligmosomoides polygyrus prior to infection with S.

Transcriptome analysis reveals human cytomegalovirus reprograms monocyte differentiation toward an M1 macrophage.

Monocytes are primary targets for human CMV (HCMV) infection and are proposed to be responsible for hematogenous dissemination of the virus. Monocytes acquire different functional traits during polarization to the classical proinflammatory M1 macrophage or the alternative antiinflammatory M2 macrophage. We hypothesized that HCMV induced a proinflammatory M1 macrophage following infection to promote viral dissemination because, biologically, a proinflammatory state provides the tools to drive infected monocytes from the blood into the tissue.

In vitro and in vivo characterization of equine herpesvirus type 1 (EHV-1) mutants devoid of the viral chemokine-binding glycoprotein G (gG).

Glycoprotein G (gG) of equine herpesvirus type 1 (EHV-1), a structural component of virions and secreted from virus-infected cells, was shown to bind to a variety of different chemokines and as such might be involved in immune modulation. Little is known, however, about its role in the replication cycle and infection of EHV-1 in vivo. Here we report on the function of gG in context of virus infection in vitro and in vivo.

Expression of the full-length form of gp2 of equine herpesvirus 1 (EHV-1) completely restores respiratory virulence to the attenuated EHV-1 strain KyA in CBA mice.

Wild-type equine herpesvirus 1 (EHV-1) strains express a large (250-kDa) glycoprotein, gp2, that is encoded by EUs4 (gene 71) located within the unique short region of the genome. DNA sequence analysis revealed that EUs4 of the pathogenic EHV-1 strain RacL11 is an open reading frame of 2,376 bp that encodes a protein of 791 amino acids. The attenuated EHV-1 vaccine strain KyA harbors an in-frame deletion of 1,242 bp from bp 222 to 1461 and expresses a truncated gp2 of 383 amino acids.

Meningoencephalitis in mice infected with an equine herpesvirus 1 strain KyA recombinant expressing glycoprotein I and glycoprotein E.

One of the consequences of equine herpesvirus 1 (EHV-1) infection in the natural host is a neurological disease that can lead to paralysis. The pathology associated with EHV-1-induced neurological disease includes vasculitis of the small blood vessels within the central nervous system and subsequent damage to the surrounding neural tissue. In a previous study, an EHV-1 recombinant KyA virus (KgI/gE/75) was generated in which the sequences encoding glycoprotein I (gI) and glycoprotein E (gE) were repaired [Frampton et al.

HCMV activates PI(3)K in monocytes and promotes monocyte motility and transendothelial migration in a PI(3)K-dependent manner.

Human cytomegalovirus (HCMV) is a leading cause of morbidity and mortality in immunocompromised hosts. In immunocompetent hosts, HCMV is associated with chronic inflammatory diseases including atherosclerosis. Monocytes and macrophages are proposed to play key roles in HCMV dissemination to host tissue, and their infection provides a biological link between the lifecycle of HCMV and disease pathology.

Cytokine profiles and long-term virus-specific antibodies following immunization of CBA mice with equine herpesvirus 1 and viral glycoprotein D.

Equine herpesvirus 1 (EHV-1)-specific antibody-secreting cells (ASC) isolated from the lung and spleen of mice at 12 months after immunization with attenuated EHV-1 KyA, heat-killed KyA, or recombinant viral glycoprotein D (rgD) assessed by ELISPOT showed a three- to fivefold increase in three immunoglobulin isotypes at 3 days post-challenge with pathogenic EHV-1 RacL11 as compared to control mice. ELISPOT assays demonstrated a high frequency of cells secreting proinflammatory tumor necrosis factor-alpha (TNF-alpha), interferon gamma (IFN-gamma), and interleukin 4 (IL-4) in the lungs in response to infection with KyA or RacL11 or immunization with rgD. Cytokine production elicited by EHV-1 KyA or RacL11 infection revealed similar frequencies of EHV-1-specific IFN-gamma and IL-4 spot forming cells in the mediastinal lymph nodes and spleen.