The origin of summer monsoon rainfall at New Delhi by deuterium excess

International audienceThe deuterium excess in summer monsoon precipitation, determined from isotopic measurements(?18O and Keywords: deuterium excess, relative humidity, origin of precipitatio

Regional genome transcriptional response of adult mouse brain to hypoxia

<p>Abstract</p> <p>Background</p> <p>Since normal brain function depends upon continuous oxygen delivery and short periods of hypoxia can precondition the brain against subsequent ischemia, this study examined the effects of brief hypoxia on the whole genome transcriptional response in adult mouse brain.</p> <p>Result</p> <p>Pronounced changes of gene expression occurred after 3 hours of hypoxia (8% O₂) and after 1 hour of re-oxygenation in all brain regions. The hypoxia-responsive genes were predominantly up-regulated in hindbrain and predominantly down-regulated in forebrain - possibly to support hindbrain survival functions at the expense of forebrain cognitive functions. The up-regulated genes had a significant role in cell survival and involved both shared and unshared signaling pathways among different brain regions. Up-regulation of transcriptional signaling including hypoxia inducible factor, insulin growth factor (IGF), the vitamin D3 receptor/retinoid X nuclear receptor, and glucocorticoid signaling was common to many brain regions. However, many of the hypoxia-regulated target genes were specific for one or a few brain regions. Cerebellum, for example, had 1241 transcripts regulated by hypoxia only in cerebellum but not in hippocampus; and, 642 (54%) had at least one hepatic nuclear receptor 4A (HNF4A) binding site and 381 had at least two HNF4A binding sites in their promoters. The data point to HNF4A as a major hypoxia-responsive transcription factor in cerebellum in addition to its known role in regulating erythropoietin transcription. The genes unique to hindbrain may play critical roles in survival during hypoxia.</p> <p>Conclusion</p> <p>Differences of forebrain and hindbrain hypoxia-responsive genes may relate to suppression of forebrain cognitive functions and activation of hindbrain survival functions, which may coordinately mediate the neuroprotection afforded by hypoxia preconditioning.</p

Assessment of soil salinisation in the Ejina Oasis located in the lower reaches of Heihe River, Northwestern China

Recognition of the spatial-temporal distribution characteristics of soil salinity has become an important basis for the formulation of strategies required in the utilisation and sustainable development of soil resources in arid and semi-arid area. In this paper, based on vegetation cover dataset during 1998–2015 in Ejina region combined with the collected soil salinity data, geostatistical methods were used to explore the temporal and spatial dynamic characteristics of soil salinity and its impact on vegetation in the study area. The results showed significant differences in soil salinisation characteristics with a large variability in the soil salinity among the different soil depths, with a variation coefficient ranging from about 0.97–1.47. Soils are represented by a continuous variation, both in space and time. Soil salinity showed an obvious spatial autocorrelation, with a plaque type distribution. The areas of the salinised soil found for the years 2003, 2011 and 2015 were approximately 18,565, 23,206 and 17,721 km2, respectively. From the relationships deduced between the normalised difference vegetation index (NDVI) and soil moisture and salt content in different soil depths, the present study ascertains that the soil moisture content is the most important limiting factor of vegetation growth in Ejina Oasis

Brain distribution and elimination of recombinant human TIMP-1 after cerebral ischemia and reperfusion in rats

bjective To investigate recombinant human TIMP-1 (125I-rhTIMP-1) half-life in blood and its distribution in rat brain tissue after cerebral ischemia/reperfusion as part of a therapeutic development paradigm. Method A suture model of the middle cerebral artery occlusion was used. 125I-labeled rhTIMP-1 at 60 μg/kg (11.23 μCi/μg) was administered to rats intravenously at the beginning of reperfusion. Blood and brain tissue were collected. The radioactivity was detected with a gamma counter and analyzed by autoradiography. Results The blood half-life T1/2 of 125I-rhTIMP-1 was 42.2 hours. Thirty minutes after 125I-rhTIMP-1 administration, an increased accumulation of 125I-rhTIMP-1 in the ischemic hemisphere was observed. The maximum brain tissue concentration Cmax was 26.1 ng/g at 1.5 hours in the striatum and 13.9 ng/g at 5 hours in the cortex when the uptake percentage of brain tissue to blood was 6.1±0.4 and 6.7±2.1%, respectively. The cortex and striatum elimination half-lives T1/2 were 45.3 and 39.2 hours, respectively. Electrophoretic analysis of ischemic samples for 125I-rhTIMP-1 showed a clear 28 kDa band 1.5 hours after 125I-rhTIMP-1 administration in the cortex and striatum. The intensity of the 28 kDa band decreased after 3.0 hours of the administration. Some 125I-rhTIMP-1 maintained its molecular integrity for 8.5 hours in ischemic striatum after reperfusion. Discussion 125I-labeled rhTIMP-1 was distributed quickly into ischemic brain tissue and had a slow elimination in both blood and brain tissue. These results, along with other studies suggesting therapeutic benefits, will aid in the development of TIMP-1 for protecting ischemic stroke

Hemorrhagic transformation after ischemic stroke in animals and humans.

Hemorrhagic transformation (HT) is a common complication of ischemic stroke that is exacerbated by thrombolytic therapy. Methods to better prevent, predict, and treat HT are needed. In this review, we summarize studies of HT in both animals and humans. We propose that early HT (&lt;18 to 24 hours after stroke onset) relates to leukocyte-derived matrix metalloproteinase-9 (MMP-9) and brain-derived MMP-2 that damage the neurovascular unit and promote blood-brain barrier (BBB) disruption. This contrasts to delayed HT (&gt;18 to 24 hours after stroke) that relates to ischemia activation of brain proteases (MMP-2, MMP-3, MMP-9, and endogenous tissue plasminogen activator), neuroinflammation, and factors that promote vascular remodeling (vascular endothelial growth factor and high-moblity-group-box-1). Processes that mediate BBB repair and reduce HT risk are discussed, including transforming growth factor beta signaling in monocytes, Src kinase signaling, MMP inhibitors, and inhibitors of reactive oxygen species. Finally, clinical features associated with HT in patients with stroke are reviewed, including approaches to predict HT by clinical factors, brain imaging, and blood biomarkers. Though remarkable advances in our understanding of HT have been made, additional efforts are needed to translate these discoveries to the clinic and reduce the impact of HT on patients with ischemic stroke

Hemorrhagic Transformation after Ischemic Stroke in Animals and Humans

Hemorrhagic transformation (HT) is a common complication of ischemic stroke that is exacerbated by thrombolytic therapy. Methods to better prevent, predict, and treat HT are needed. In this review, we summarize studies of HT in both animals and humans. We propose that early HT (<18 to 24 hours after stroke onset) relates to leukocyte-derived matrix metalloproteinase-9 (MMP-9) and brain-derived MMP-2 that damage the neurovascular unit and promote blood–brain barrier (BBB) disruption. This contrasts to delayed HT (>18 to 24 hours after stroke) that relates to ischemia activation of brain proteases (MMP-2, MMP-3, MMP-9, and endogenous tissue plasminogen activator), neuroinflammation, and factors that promote vascular remodeling (vascular endothelial growth factor and high-moblity-group-box-1). Processes that mediate BBB repair and reduce HT risk are discussed, including transforming growth factor beta signaling in monocytes, Src kinase signaling, MMP inhibitors, and inhibitors of reactive oxygen species. Finally, clinical features associated with HT in patients with stroke are reviewed, including approaches to predict HT by clinical factors, brain imaging, and blood biomarkers. Though remarkable advances in our understanding of HT have been made, additional efforts are needed to translate these discoveries to the clinic and reduce the impact of HT on patients with ischemic stroke