217 research outputs found

    Palaeoan Thropological Study Of Late Prehistoric Human Skeletal Remains In Semporna, Sabah [Cc1-960]

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    Penyelidikan arkeologi di Semporna, Sabah dari tahun 2002 hingga 2007 telah menemui dua tapak pengkebumian Zaman Akhir Prasejarah di Melanta Tutup dan Bukit Kamiri. Archaeological research in Semporna, Sabah in 2002 to 2007 uncovered two burial sites in Melanta Tutup and Bukit Kamiri dated to the Late Prehistoric period

    Complete mitochondrial DNA genome variation in Peninsular Malaysia

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    The peopling of Southeast Asia has been vigorously debated over the past few decades by archaeologists, linguists and anthropologists, as well as evolutionary and population geneticists. Several ethnic minorities in the region, the Orang Asli groups (the Semang, Senoi and Aboriginal Malays) from Peninsular Malaysia, are widely thought of as “relicts” of human diversity in the ancient Sunda continent. However, mitochondrial DNA (mtDNA analysis of these groups has hitherto been restricted to a small number of populations and largely based on the mtDNA control region hypervariable segment I (HVS-I), supplemented by a very small number of whole-mtDNA genomes. In this study, I have both expanded the number of populations examined and analysed 226 lineages at the level of whole-mtDNA genomes from both Orang Asli and modern Malay populations, covering most of the extant mtDNA diversity in Peninsular Malaysia, in the context of Southeast Asian variation more generally, including a total of 2206 complete mtDNA sequences in the phylogeographic analysis. This has confirmed that the Orang Asli populations indeed experienced high genetic drift, likely due to their extremely small group sizes and population subdivision. All three Orang Asli groups have local roots that trace back to ~50 ka, and all have been affected to a greater or lesser extent by subsequent migrations to Peninsular Malaysia. The Semang and Senoi show much less haplogroup diversity than the Aboriginal Malays, although the latter have some indigenous ancestry that is as deep as that of the Semang and Senoi in Peninsular Malaysia. However, this drift, and the loss of lineages that it has entailed, is compensated for by the retention of many related ancient lineages in the extant modern Malay, who therefore provide a more comprehensive view of ancient Malay Peninsula, and more generally ancient Sunda, mtDNA diversity. Indeed, contrary to the model that posits a recent ancestry for Malay in Island Southeast Asia (ISEA), a majority of their maternal lineages appear to have had a local ancestry within Mainland Southeast Asia (MSEA) and the Malay Peninsula. Combining the Orang Asli and Malay data indicates a very deep ancestry for multiple indigenous maternal lineages that date back locally (or regionally) to the late Pleistocene. Many can be traced to the original inhabitants of Southeast Asia, who colonised the Sunda region from South Asia ~50–60 ka. It appears that the spread of the so-called “Coastal Neolithic” foraging groups (who may have engaged in horticulture, but were largely pre-rice agriculture) may have provided the main contribution to the north–south lineage expansions and the spread of Austro-Asiatic languages to the Orang Asli and to the Nicobars may be connected to some of these dispersals. Apart from preserving these ancient lineages, many of which have been lost by drift in the relict populations, the modern Malay also preserve complex maternal influences from further afield at various times stretching back to the Last Glacial Maximum, from ISEA (as far east as the New Guinea region), to a lesser extent from East Asia, and to an even lesser extent South Asia. Climatic change and sea-level rises were likely the most important driving force behind the demographic history of Southeast Asia, mainland as well as insular, as shown by a sharp signal of early Holocene population crash and subsequent re-expansion in both the modern Malay and the Orang Asli. Although there is substantial lineage sharing between modern Malay and their close Sunda neighbours in Sumatra, ISEA lineages amount to little more than a quarter of the maternal variation of Malay, and even if there was a major migration to the Peninsula in the Late Holocene, the majority of their maternal ancestry seems to lie within the bounds of the Sunda continent

    Spatiotemporal changes in biomass after selective logging in a lowland tropical rainforest in peninsular Malaysia

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    We studied biomass changes in a lowland tropical rain forest in the Pasoh Forest Reserve of Peninsular Malaysia after selective logging in 1958. A tree census was undertaken every 2 years from 1998 to 2012 in a 6-ha logged forest plot. Total aboveground biomass (AGB) was 72 % of that in a primary forest plot within the same reserve in 1998, but reached 87 % in 2012. AGB regrowth was spatially variable within the logged forest plot and was much less in swampy areas than in upland areas. The overall annual growth rate of AGB in the logged forest throughout the study period was 1.5 % and slowed (to 0.6 %) in a dry period (2004-2006). The biomass of large trees (DBH ≥ 50 cm) increased by 56 % during the study period, but amounted to only 58 % of the biomass of the corresponding size class in the primary forest, suggesting that stand structure is still recovering from logging. Spatiotemporal variation in AGB recovery after logging needs to be taken into account for logging and subsequent management of the tropical lowland forest biome

    Mechanisms of oligodendrocyte regeneration from ventricular-subventricular zone-derived progenitor cells in white matter diseases

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    White matter dysfunction is an important part of many CNS disorders including multiple sclerosis (MS) and vascular dementia. Within injured areas, myelin loss and oligodendrocyte death may trigger endogenous attempts at regeneration. However, during disease progression, remyelination failure may eventually occur due to impaired survival/proliferation, migration/recruitment, and differentiation of oligodendrocyte precursor cells (OPCs). The ventricular-subventricular zone (V-SVZ) and the subgranular zone (SGZ) are the main sources of neural stem/progenitor cells (NSPCs), which can give rise to neurons as well as OPCs. Under normal conditions in the adult brain, the V-SVZ progenitors generate a large number of neurons with a small number of oligodendrocyte lineage cells. However, after demyelination, the fate of V-SVZ-derived progenitor cells shifts from neurons to OPCs, and these newly generated OPCs migrate to the demyelinating lesions to ease white matter damage. In this mini-review, we will summarize the recent studies on extrinsic (e.g., vasculature, extracellular matrix (ECM), cerebrospinal fluid (CSF)) and intrinsic (e.g., transcription factors, epigenetic modifiers) factors, which mediate oligodendrocyte generation from the V-SVZ progenitor cells. A deeper understanding of the mechanisms that regulate the fate of V-SVZ progenitor cells may lead to new therapeutic approaches for ameliorating white matter dysfunction and damage in CNS disorders

    Intravenous tPA therapy does not worsen acute intracerebral hemorrhage in mice

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    Tissue plasminogen activator (tPA) is the only FDA-approved treatment for reperfusing ischemic strokes. But widespread use of tPA is still limited by fears of inadvertently administering tPA in patients with intracerebral hemorrhage (ICH). Surprisingly, however, the assumption that tPA will worsen ICH has never been biologically tested. Here, we assessed the effects of tPA in two models of ICH. In a mouse model of collagenase-induced ICH, hemorrhage volumes and neurological deficits after 24 hrs were similar in saline controls and tPA-treated mice, whereas heparin-treated mice had 3-fold larger hematomas. In a model of laser-induced vessel rupture, tPA also did not worsen hemorrhage volumes, while heparin did. tPA is known to worsen neurovascular injury by amplifying matrix metalloproteinases during cerebral ischemia. In contrast, tPA did not upregulate matrix metalloproteinases in our mouse ICH models. In summary, our experimental data do not support the assumption that intravenous tPA has a deleterious effect in acute ICH. However, due to potential species differences and the inability of models to fully capture the dynamics of human ICH, caution is warranted when considering the implications of these findings for human therapy

    Combination therapy with normobaric oxygen (NBO) plus thrombolysis in experimental ischemic stroke

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    <p>Abstract</p> <p>Background</p> <p>The widespread use of tissue plasminogen activator (tPA), the only FDA-approved acute stroke treatment, remains limited by its narrow therapeutic time window and related risks of brain hemorrhage. Normobaric oxygen therapy (NBO) may be a useful physiological strategy that slows down the process of cerebral infarction, thus potentially allowing for delayed or more effective thrombolysis. In this study we investigated the effects of NBO started simultaneously with intravenous tPA, in spontaneously hypertensive rats subjected to embolic middle cerebral artery (MCA) stroke. After homologous clot injection, animals were randomized into different treatment groups: saline injected at 1 hour; tPA at 1 hour; saline at 1 hour plus NBO; tPA at 1 hour plus NBO. NBO was maintained for 3 hours. Infarct volume, brain swelling and hemorrhagic transformation were quantified at 24 hours. Outcome assessments were blinded to therapy.</p> <p>Results</p> <p>Upon clot injection, cerebral perfusion in the MCA territory dropped below 20% of pre-ischemic baselines. Both tPA-treated groups showed effective thrombolysis (perfusion restored to nearly 100%) and smaller infarct volumes (379 ± 57 mm<sup>3 </sup>saline controls; 309 ± 58 mm<sup>3 </sup>NBO; 201 ± 78 mm<sup>3 </sup>tPA; 138 ± 30 mm<sup>3 </sup>tPA plus NBO), showing that tPA-induced reperfusion salvages ischemic tissue and that NBO does not significantly alter this neuroprotective effect. NBO had no significant effect on hemorrhagic conversion, brain swelling, or mortality.</p> <p>Conclusion</p> <p>NBO can be safely co-administered with tPA. The efficacy of tPA thrombolysis is not affected and there is no induction of brain hemorrhage or edema. These experimental results require clinical confirmation.</p

    Prospectus, April 25, 1973

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    NEW STUGO REPRESENTATIVES; 4-day nutrition workshop; Student\u27s views sought; Broken Hearts; Junior college visitation day; Student to give report to Academy; May elected chairman of nurse ass\u27n; Day Senator: Brenda Kendricks; Day Senator: Earnest Hite; Day Senator: Ken Segan; Convocations: Bill Tigrak; United Farm Workers organize boycotts; To the Editor; Brenda and Leroy; Judging teams; Festival; haiku; poem; incentive; Women welcome!; AAUW Scholarship awarded; Bridge tourney; bullet; Magical Mystery Tour: A quickie visit to Parkland\u27s new campus; What would you like to know about the new campus?; Prof Spectus; \u27How dare you presume I\u27m straight?\u27 Notes of a lesbian; PC bowlers romp to victory in 1st central Illinois tourney; From above an athlete\u27s feet; What\u27s decent to eat?; Baseballers win three of four games; Track team has high hopes; Changes in PC athletics; Thinclads take third; Wrestlinghttps://spark.parkland.edu/prospectus_1973/1008/thumbnail.jp

    Role of Hypoxic OPC in Angiogenesis

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    Background-Oligodendrocyte precursor cells (OPCs) regulate neuronal, glial, and vascular systems in diverse ways and display phenotypic heterogeneity beyond their established role as a reservoir for mature oligodendrocytes. However, the detailed phenotypic changes of OPCs after cerebral ischemia remain largely unknown. Here, we aimed to investigate the roles of reactive OPCs in the ischemic brain. Methods and Results-The behavior of OPCs was evaluated in a mouse model of ischemic stroke produced by transient middle cerebral artery occlusion in vivo. For in vitro experiments, the phenotypic change of OPCs after oxygen glucose derivation was examined using a primary rat OPC culture. Furthermore, the therapeutic potential of hypoxic OPCs was evaluated in a mouse model of middle cerebral artery occlusion in vivo. Perivascular OPCs in the cerebral cortex were increased alongside poststroke angiogenesis in a mouse model of middle cerebral artery occlusion. In vitro RNA‐seq analysis revealed that primary cultured OPCs increased the gene expression of numerous pro‐angiogenic factors after oxygen glucose derivation. Hypoxic OPCs secreted a greater amount of pro‐angiogenic factors, such as vascular endothelial growth factor and angiopoietin‐1, compared with normoxic OPCs. Hypoxic OPC‐derived conditioned media increased the viability and tube formation of endothelial cells. In vivo studies also demonstrated that 5 consecutive daily treatments with hypoxic OPC‐conditioned media, beginning 2 days after middle cerebral artery occlusion, facilitated poststroke angiogenesis, alleviated infarct volume, and improved functional disabilities. Conclusions-Following cerebral ischemia, the phenotype of OPCs in the cerebral cortex shifts from the parenchymal subtype to the perivascular subtype, which can promote angiogenesis. The optimal use of hypoxic OPCs secretome would provide a novel therapeutic option for stroke
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