内蒙古草地挥发性有机物的预研究

内蒙古草原挥发性有机物的研究在大气化学、大气环境领域具有重要的作用。2001年夏季,利用便携式光离子化检测器以及采样仪器对于内蒙古草原的一些优势草种进行了测量,得到了对内蒙古草原挥发性有机物的初步认识。     

Activation of protease-activated receptor (PAR) 1 by frog trefoil factor (TFF) 2 and PAR4 by human TFF2

Trefoil factors (TFFs) promote epithelial cell migration to reseal superficial wounds after mucosal injury, but their receptors and the molecular mechanisms underlying this process are poorly understood. In this study, we showed that frog TFF2 activates protease-activated receptor (PAR) 1 to induce human platelet aggregation. Based on this result, we further tested the involvement of PARs in human TFF2 (hTFF2)-promoted mucosal healing. hTFF2-stimulated migration of epithelial HT-29 cells was largely inhibited by PAR4 depletion with small interfering RNAs but not by PAR1 or PAR2 depletion. The PAR4-negative epithelial cell lines AGS and LoVo were highly responsive to hTFF2 as assessed by phosphorylation of ERK1/2 and cell migration upon PAR4 expression. Our findings suggest that hTFF2 promotes cell migration via PAR4. These findings will be helpful in further investigations into the functions and molecular mechanisms of TFFs and PARs in physiology and disease.     

Multiple self-healing squamous epithelioma is caused by a disease-specific spectrum of mutations in TGFBR1

Multiple self-healing squamous epithelioma (MSSE), also known as Ferguson-Smith disease (FSD), is an autosomal-dominant skin cancer condition characterized by multiple squamous-carcinoma-like locally invasive skin tumors that grow rapidly for a few weeks before spontaneously regressing, leaving scars. High-throughput genomic sequencing of a conservative estimate (24.2 Mb) of the disease locus on chromosome 9 using exon array capture identified independent mutations in TGFBR1 in three unrelated families. Subsequent dideoxy sequencing of TGFBR1 identified 11 distinct monoallelic mutations in 18 affected families, firmly establishing TGFBR1 as the causative gene. The nature of the sequence variants, which include mutations in the extracellular ligand-binding domain and a series of truncating mutations in the kinase domain, indicates a clear genotype-phenotype correlation between loss-of-function TGFBR1 mutations and MSSE. This distinguishes MSSE from the Marfan syndrome-related disorders in which missense mutations in TGFBR1 lead to developmental defects with vascular involvement but no reported predisposition to cancer.     

The regulatory function of SPARC in vascular biology

SPARC is a matricellular protein, able to modulate cell/ECM interactions and influence cell responses to growth factors, and therefore is particularly attuned to contribute to physiological processes involving changes in ECM and cell mobilization. Indeed, the list of biological processes affected by SPARC includes wound healing, tumor progression, bone formation, fibrosis, and angiogenesis. The process of angiogenesis is complex and involves a number of cellular processes such as endothelial cell proliferation, migration, ECM degradation, and synthesis, as well as pericyte recruitment to stabilize nascent vessels. In this review, we will summarize current results that explore the function of SPARC in the regulation of angiogenic events with a particular emphasis on the modulation of growth factor activity by SPARC in the context of blood vessel formation. The primary function of SPARC in angiogenesis remains unclear, as SPARC activity in some circumstances promotes angiogenesis and in others is more consistent with an anti-angiogenic activity. Undoubtedly, the mercurial nature of SPARC belies a redundancy of functional proteins in angiogenesis as well as cell-type-specific activities that alter signal transduction events in response to unique cellular milieus. Nonetheless, the investigation of cellular mechanisms that define functional activities of SPARC continue to contribute novel and exciting paradigms to vascular biology.     

Protein O-GlcNAcylation regulates Drosophila growth through the insulin signaling pathway

Modification of nuclear and cytosolic proteins by O-linked N-acetylglucosamine (O-GlcNAcylation) is ubiquitous in cells. The in vivo function of the protein O-GlcNAcylation, however, is not well understood. Here, we manipulated the cellular O-GlcNAcylation level in Drosophila and found that it promotes developmental growth by enhancing insulin signaling. This increase in growth is due mainly to cell growth and not to cell proliferation. Our data suggest that the increase in the insulin signaling activity is mediated, at least in part, through O-GlcNAcylation of Akt. These results indicate that O-GlcNAcylation is one of the crucial mechanisms involved in control of insulin signaling during Drosophila development.     

Amyloid β-induced FOXRED2 mediates neuronal cell death via inhibition of proteasome activity

Proteasome inhibition has been regarded as one of the mediators of Aβ neurotoxicity. In this study, we found that FOXRED2, a novel endoplasmic reticulum (ER) residential protein, is highly up-regulated by Aβ in rat cortical neurons and SH-SY5Y cells. Over-expression of FOXRED2 inhibits proteasome activity in the microsomal fractions containing ER and interferes with proteasome assembly, as evidenced by gel filtration and native gel electrophoresis analysis. In contrast, reduced expression of FOXRED2 rescues Aβ-induced inhibition of proteasome activity. FOXRED2 is an unstable protein with two degradation boxes and one KEN box, and its N-terminal oxidoreductase domain is required for proteasome inhibition. Ectopic expression of FOXRED2 induces ER stress-mediated cell death via caspase-12, which is inhibited by Salubrinal. Further, down-regulation of FOXRED2 expression attenuates Aβ-induced cell death and the ER stress response. These results suggest that up-regulated FOXRED2 inhibits proteasome activity by interfering with 26S proteasome assembly to contribute to Aβ neurotoxicity via an ER stress response.     

Phylogenetic taxonomy of Hemiphyllodactylus Bleeker, 1860 (Squamata: Gekkonidae) with descriptions of three new species from Myanmar

ABSTRACT

A phylogenetic taxonomy of the gekkonid genus Hemiphyllodactylus based on molecular, morphological, and ecological data recovered 28 species, including three new species from the upland regions of the Shan Plateau in eastern Myanmar. Hemiphyllodactylus linnwayensis sp. nov. is a forest-adapted species that may also be a human commensal and H. montawaensis sp. nov. and H. tonywhitteni sp. nov. are karst forest-adapted species. The discovery of three new species from montane regions in eastern Myanmar extends the distribution of a larger monophyletic group of Hemiphyllodactylus westward to the eastern edge of the Ayeyrawady Basin through a series of semi-contiguous, parallel mountain ranges originating in western China and northern Thailand. The discovery of the karst forest-adapted H. montawaensis sp. nov. and H. tonywhitteni sp. nov. further emphasizes the unrealized herpetological diversity endemic to karst ecosystems and the need for increased field work throughout such habitats in South-East Asia.

www.zoobank.org/urn:lsid:zoobank.org:pub:E42FA075-E8E0-4005-98AB-12E8D5F23A07     

Eight new species of the genus Promalactis (Lepidoptera: Oecophoridae) from Indonesia,with a checklist of the genus

Eight new species of Promalactis were discovered from Indonesia: Promalactis diazomatis sp. nov., Promalactis hamatella sp. nov., Promalactis ingenticula sp. nov., Promalactis laetusella sp. nov., Promalactis latifundus sp. nov., Promalactis minutispina sp. nov., Promalactis mooatana sp. nov. and Promalactis trigonilancis sp. nov. Illustrations of adults and genitalia of the new species and taxonomic information for the six previously known species from Indonesia are provided. A checklist of the genus in Indonesia is given.

www.zoobank.org/urn:lsid:zoobank.org:pub:E25224C7-2D41-4F5A-A4BB-41AA1307E0C0     

Why Should We Be Pessimistic About Antirealists and Pessimists?

The pessimistic induction over scientific theories (Poincaré in Science and hypothesis, Dover, New York, 1905/1952) holds that present theories will be overthrown as were past theories. The pessimistic induction over scientists (Stanford in Exceeding our grasp: science, history, and the problem of unconceived alternatives, Oxford University Press, Oxford, 2006) holds that present scientists cannot conceive of future theories just as past scientists could not conceive of present theories. The pessimistic induction over realists (Wray in Synthese 190(18):4321–4330, 2013) holds that present realists are wrong about present theories just as past realists were wrong about past theories. The pessimistic induction over antirealist theories (Park in Organon F 21(1):3–21, 2014) holds that the latest antirealist explanation of the success of science (Lyons in Philos Sci 70(5):891–901, 2003) has hidden problems just as its eight predecessors did. In this paper, I (1) criticize the pessimistic inductions over scientific theories, scientists, and realists, (2) introduce a pessimistic induction over antirealist theories, and then (3) construct two new pessimistic inductions. One is a pessimistic induction over antirealists according to which the author of the latest antirealist proposal cannot see hidden problems with his proposal just as his antirealist predecessors could not see hidden problems with their proposals. The other is the pessimistic induction over pessimists according to which since past pessimists have been wrong about their present scientific theories from the early twentieth century to the early twenty-first century, future pessimists will also be wrong about their present scientific theories from the early twenty-first century to the early twenty-second century.     

Identification of common variants associated with human hippocampal and intracranial volumes

Identifying genetic variants influencing human brain structures may reveal new biological mechanisms underlying cognition and neuropsychiatric illness. The volume of the hippocampus is a biomarker of incipient Alzheimer's disease and is reduced in schizophrenia, major depression and mesial temporal lobe epilepsy. Whereas many brain imaging phenotypes are highly heritable, identifying and replicating genetic influences has been difficult, as small effects and the high costs of magnetic resonance imaging (MRI) have led to underpowered studies. Here we report genome-wide association meta-analyses and replication for mean bilateral hippocampal, total brain and intracranial volumes from a large multinational consortium. The intergenic variant rs7294919 was associated with hippocampal volume (12q24.22; N = 21,151; P = 6.70 × 10(-16)) and the expression levels of the positional candidate gene TESC in brain tissue. Additionally, rs10784502, located within HMGA2, was associated with intracranial volume (12q14.3; N = 15,782; P = 1.12 × 10(-12)). We also identified a suggestive association with total brain volume at rs10494373 within DDR2 (1q23.3; N = 6,500; P = 5.81 × 10(-7)).