Hiding Amongst the Palms: the Remarkable Discovery of a New Palm Bug Genus and Species (Insecta: Heteroptera: Thaumastocoridae: Xylastodorinae) from Remote Norfolk Island; its Systematics, Natural History, Palm Specialism and Biogeography

he discovery of a remarkable new palm bug species on Norfolk Island brings into question its systematic position within the family Thaumastocoridae, and the validity and biogeography of the three extant subfamilies. Latebracoris norfolcensis gen. nov., sp. nov. is described from remote Norfolk Island in the Southwest Pacific. The species was found on the native Norfolk Island palm Rhopalostylis baueri. The formal description of the species includes fine details of external non-genitalic and genitalic characters, supported with images from light and scanning electron microscopy. Details of the egg are described, including the shape and micropylar configuration. All nymphal stages are diagnosed morphologically and morphometrically, with the segregation of the five instars using the Brooks–Dyar Rule. The natural history of the Norfolk Island Palm Bug is documented, including the oviposition site of eggs, and microhabitat of nymphs and adults on palm infructescences, with hypotheses about development in relation to reproductive succession of the palm host. The systematic position of the Norfolk Island Palm Bug is assessed through a phylogenetic analysis of a selection of taxa of the superfamily Miroidea, using the parsimony criterion. The phylogenetic analyses were partitioned into Recent and fossil taxa, revealing monophyly of the Thaumastocoridae, and the subfamilies Thaumastocorinae and Xylastodorinae, with synapomorphy and significant resampling support. The Thaicorinae are verified as synonymous with the Xylastodorinae. The monotypic fossil subfamily Thaumastotinginae is removed from the Thaumastocoridae and treated as incertae familiae. Suprageneric relationships were corroborated in the two taxon partition analyses. An overview of host associations is given verifying palm specialism for the Xylastodorinae. The natural history, palm specialism, biogeography, morphology and systematics of the Xylastodorinae and allies are discussed in light of the discovery of Latebracoris norfolcensis

Phospholipid composition and kinetics in different endobronchial fractions from healthy volunteers

Tracheal secretions may be of value as a surrogate to assess bronchoalveolar lavage fluid surfactant molecular composition and metabolism in healthy people. Despite minor differences, the phospholipid molecular composition of induced sputum also showed similarities to that of bronchoalveolar lavage fluid. Detailed analysis of newly synthesized individual phosphatidylcholine species provided novel insights into mechanisms of surfactant synthesis and acyl remodelling. Lysophosphatidylcholine methyl-D9 incorporation patterns suggest that these species are secreted together with other surfactant phospholipids and are not generated in the air spaces by hydrolysis of secreted surfactant phosphatidylcholine. Application into patient populations may elucidate potential underlying pathophysiological mechanisms that lead to surfactant alterations in disease state

Antioxidant Role for Lipid Droplets in a Stem Cell Niche of Drosophila

SummaryStem cells reside in specialized microenvironments known as niches. During Drosophila development, glial cells provide a niche that sustains the proliferation of neural stem cells (neuroblasts) during starvation. We now find that the glial cell niche also preserves neuroblast proliferation under conditions of hypoxia and oxidative stress. Lipid droplets that form in niche glia during oxidative stress limit the levels of reactive oxygen species (ROS) and inhibit the oxidation of polyunsaturated fatty acids (PUFAs). These droplets protect glia and also neuroblasts from peroxidation chain reactions that can damage many types of macromolecules. The underlying antioxidant mechanism involves diverting PUFAs, including diet-derived linoleic acid, away from membranes to the core of lipid droplets, where they are less vulnerable to peroxidation. This study reveals an antioxidant role for lipid droplets that could be relevant in many different biological contexts

Multiomics links global surfactant dysregulation with airflow obstruction and emphysema in COPD

RATIONALE: Pulmonary surfactant is vital for lung homeostasis as it reduces surface tension to prevent alveolar collapse and provides essential immune-regulatory and antipathogenic functions. Previous studies demonstrated dysregulation of some individual surfactant components in COPD. We investigated relationships between COPD disease measures and dysregulation of surfactant components to gain new insights into potential disease mechanisms. METHODS: Bronchoalveolar lavage proteome and lipidome were characterised in ex-smoking mild/moderate COPD subjects (n=26) and healthy ex-smoking (n=20) and never-smoking (n=16) controls using mass spectrometry. Serum surfactant protein analysis was performed. RESULTS: Total phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol, surfactant protein (SP)-B, SP-A and SP-D concentrations were lower in COPD versus controls (log2 fold change (log2FC) -2.0, -2.2, -1.5, -0.5, -0.7 and -0.5 (adjusted p<0.02), respectively) and correlated with lung function. Total phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol, SP-A, SP-B, SP-D, napsin A and CD44 inversely correlated with computed tomography small airways disease measures (expiratory to inspiratory mean lung density) (r= -0.56, r= -0.58, r= -0.45, r= -0.36, r= -0.44, r= -0.37, r= -0.40 and r= -0.39 (adjusted p<0.05)). Total phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol, SP-A, SP-B, SP-D and NAPSA inversely correlated with emphysema (% low-attenuation areas): r= -0.55, r= -0.61, r= -0.48, r= -0.51, r= -0.41, r= -0.31 and r= -0.34, respectively (adjusted p<0.05). Neutrophil elastase, known to degrade SP-A and SP-D, was elevated in COPD versus controls (log2FC 0.40, adjusted p=0.0390), and inversely correlated with SP-A and SP-D. Serum SP-D was increased in COPD versus healthy ex-smoking volunteers, and predicted COPD status (area under the curve 0.85). CONCLUSIONS: Using a multiomics approach, we demonstrate, for the first time, global surfactant dysregulation in COPD that was associated with emphysema, giving new insights into potential mechanisms underlying the cause or consequence of disease

A computational framework for complex disease stratification from multiple large-scale datasets.

BACKGROUND: Multilevel data integration is becoming a major area of research in systems biology. Within this area, multi-'omics datasets on complex diseases are becoming more readily available and there is a need to set standards and good practices for integrated analysis of biological, clinical and environmental data. We present a framework to plan and generate single and multi-'omics signatures of disease states. METHODS: The framework is divided into four major steps: dataset subsetting, feature filtering, 'omics-based clustering and biomarker identification. RESULTS: We illustrate the usefulness of this framework by identifying potential patient clusters based on integrated multi-'omics signatures in a publicly available ovarian cystadenocarcinoma dataset. The analysis generated a higher number of stable and clinically relevant clusters than previously reported, and enabled the generation of predictive models of patient outcomes. CONCLUSIONS: This framework will help health researchers plan and perform multi-'omics big data analyses to generate hypotheses and make sense of their rich, diverse and ever growing datasets, to enable implementation of translational P4 medicine

Aspects of hormonal regulation of hepatic carbohydrate and lipid metabolism

The liver is a major site in the rat for conversion of dietary carbohydrateinto glycogen and triglyceride. Hepatic rates of fatty acid andglycogen synthesis were measured y vivo in response to meal-feeding(2h/day) by the incorporation of from 3H20. This technique has notbeen applied previously to glycogen synthesis and was validated in controland streptozotocin diabetic rats* Hepatic glycogen recycling was low infed adult rats but was apparently greater in foetal rats. The precursorsource for glycogen synthesis in vivo could not be determined from thedistribution pattern of 3H incorporation. Hepatic glycogen synthesis waselevated in control rats for 5h after feeding. During this phase,glycogen could not have been a net precursor for other synthetic pathways®Hepatic fatty acid synthesis in control rats increased 20-fold 2h afterfeeding. This response was impaired and delayed, but not abolished, bystreptozotocin diabetes (55mg/kg). Insulin pretreatment (30 P.Z.I.)restored the low diabetic rate of lipogenesis to normal by 8h afterfeeding. Streptozotocin reduced the hepatic Vmax activities of glucokinase,ATP-citrate lyase and total acetyl CoA carboxylase. None of theseenzyme activities increased when hepatic fatty acid synthesis was stimulatedby feeding in control rats or by feeding and insulin in diabeticrats. Feeding stimulated active acetyl CoA carboxylase in control, butnot diabetic, rats. The regulation of hepatic fatty acid synthesis byboth acetyl CoA carboxylase and increased substrate concentration isdiscussed.In control rats for the first 5h after feeding, hepatic glycogen couldnot have been a net fatty acid precursor. Thus the inhibition of hepaticfatty acid synthesis in this period by glucagon (Img/kg) could not havebeen directly due to depletion of glycogen® The glucagon inhibition oflipogenesis was abolished by adrenalectomy but not potentiated bycorticotropin-treatment, suggesting a permissive role for glucocorticoidhormones. Adrenalectomy also impaired the inhibition of hepatic pyruvatekinase by glucagon but did not abolish the inactivation of pyruvatekinase by 10 )jM-cyclic AMP in vitro« The involvement of L-type pyruvatekinase in the regulation of hepatic fatty acid synthesis is discussed.The integrated regulation of the hepatic pathways of lipogenesis,glycolysis, gluconeogenesis and ketogenesis is considered

Analysis of lung surfactant phosphatidylcholine metabolism in transgenic mice using stable isotopes

Stable isotope labelling of lipid precursors coupled with mass spectrometry-based lipidomic analyses and determination of isotope enrichment in substrate, intermediate and product pools provide the parameters needed to determine absolute flux rates through lipid pathways in vivo. Here, as an illustration of the power of such analyses we investigated lung phosphatidylcholine (PC) synthesis in Surfactant Protein-D (SP-D) null mice. These animals develop emphysema, foamy alveolar macrophages and an alveolar lipoproteinosis with increasing age. We used the incorporation of methyl-9-[2H] choline chloride coupled with ESI-MS/MS to quantify absolute rates of lung surfactant PC synthesis and secretion in an SP-D-/? mouse model, together with an analysis of the molecular specificity of lung PC synthesis. PC synthetic rates were comparable in control (0.52 ?moles/lung/h) and SP-D-/? (0.69 ?moles/lung/h) mice, as were rates of surfactant PC secretion (29.8 and 30.6 nmoles/lung/h respectively). Increased lung PC in the SP-D-/? mouse was due to impaired catabolism, with a rate of accumulation of 0.057 ?moles/lung/h. The relatively low rates of surfactant PC secretion compared with total lung PC synthesis were compatible with a suggested ABCA1-mediated basolateral lipid efflux from alveolar type II epithelial cells. Finally, PC molecular species analysis suggested that a proportion of newly-synthesised PC is secreted rapidly into the lung air spaces in both control and SP-D-/? mice before significant PC acyl remodelling occurs<br/