Timing of post–Karoo alkaline volcanism in southern Namibia

1990 ◽  
Vol 127 (5) ◽  
pp. 427-433 ◽  
Author(s):  
D. L. Reid ◽  
A. F. Cooper ◽  
D. C. Rex ◽  
R. E. Harmer

AbstractNew radiometric age data are reported for alkaline centres in southern Namibia, and are discussed together with published age data in terms of models put forward to account for post-Karoo (Mesozoic–Recent) alkaline magmatism within the African plate. Agreement between K–Ar and Rb–Sr ages indicate emplacement of the Dicker Willem carbonatite in southern Namibia at 49 ± 1 Ma. Alkaline rocks associated with the Gross Brukkaros volcano show a discordant radiometric age pattern, but the best estimate for the age of this complex is 77 ± 2 Ma, similar to that obtained for the neighbouring Gibeon carbonatite-kimberlite province. The Dicker Willem carbonatite is therefore younger than the Luderitz alkaline province (133 ± 2 Ma), and the Gross Brukkaros volcano, but is older than the Klinghardt phonolite field (29–37 Ma). The new age data argue against a distinct periodicity in alkaline igneous activity in southern Africa, thereby ruling out possible controls by episodic marginal upwarping of the subcontinent. Although the available age data do not appear to be consistent with the passage of one or even two hotspots under southern Namibia, it is argued that the surface expression of hotspots under continents may be so large and overlapping that within-plate magmatism attributed to these thermal anomalies need not necessarily be confined to narrow linear belts or show an age progression. The role of hotspots in continental alkaline magmatism is most likely one of melt generation, while local crustal structure probably controls the distribution and timing of eruption. Major tectonic boundaries in the Precambrian basement underlying southern Namibia seem to have controlled the development of Tertiary alkaline centres in that region.

Author(s):  
Lotte Melchior Larsen ◽  
David C. Rex ◽  
W. Stuart Watt ◽  
Philip G. Guise

NOTE: This article was published in a former series of GEUS Bulletin. Please use the original series name when citing this article, for example: Melchior Larsen, L., Rex, D. C., Watt, W. S., & Guise, P. G. (1999). 40Ar–39Ar dating of alkali basaltic dykes along the southwest coast of Greenland: Cretaceous and Tertiary igneous activity along the eastern margin of the Labrador Sea. Geology of Greenland Survey Bulletin, 184, 19-29. https://doi.org/10.34194/ggub.v184.5227 _______________ A 380 km long coast-parallel alkali basalt dyke swarm cutting the Precambrian basement in south-western Greenland has generally been regarded as one of the earliest manifestations of rifting during continental stretching prior to break-up in the Labrador Sea. Therefore, the age of this swarm has been used in models for the evolution of the Labrador Sea, although it has been uncertain due to earlier discrepant K–Ar dates. Two dykes from this swarm situated 200 km apart have now been dated by the 40Ar–39Ar step-heating method. Separated biotites yield plateau ages of 133.3 ± 0.7 Ma and 138.6 ± 0.7 Ma, respectively. One of the dykes has excess argon. Plagioclase separates confirm the biotite ages but yield less precise results. The age 133– 138 Ma is earliest Cretaceous, Berriasian to Valanginian, and the dyke swarm is near-coeval with the oldest igneous rocks (the Alexis Formation) on the Labrador shelf. A small swarm of alkali basalt dykes in the Sukkertoppen (Maniitsoq) region of southern West Greenland was also dated. Two separated kaersutites from one sample yield an average plateau age of 55.2 ± 1.2 Ma. This is the Paleocene–Eocene boundary. The swarm represents the only known rocks of that age within several hundred kilometres and may be related to changes in the stress regime during reorganisation of plate movements at 55 Ma when break-up between Greenland and Europe took place.


2011 ◽  
Vol 300 (5) ◽  
pp. L781-L789 ◽  
Author(s):  
Szabolcs Bertok ◽  
Michael R. Wilson ◽  
Anthony D. Dorr ◽  
Justina O. Dokpesi ◽  
Kieran P. O'Dea ◽  
...  

TNF plays a crucial role in the pathogenesis of acute lung injury. However, the expression profile of its two receptors, p55 and p75, on pulmonary endothelium and their influence on TNF signaling during lung microvascular inflammation remain uncertain. Using flow cytometry, we characterized the expression profile of TNF receptors on the surface of freshly harvested pulmonary endothelial cells (PECs) from mice and found expression of both receptors with dominance of p55. To investigate the impact of stimulating individual TNF receptors, we treated wild-type and TNF receptor knockout mice with intravenous TNF and determined surface expression of adhesion molecules (E-selectin, VCAM-1, ICAM-1) on PECs by flow cytometry. TNF-induced upregulation of all adhesion molecules was substantially attenuated by absence of p55, whereas lack of p75 had a similar but smaller effect that varied between adhesion molecules. Selective blockade of individual TNF receptors by specific antibodies in wild-type primary PEC culture confirmed that the in vivo findings were due to direct effects of TNF receptor inhibition on endothelium and not other cells (e.g., circulating leukocytes). Finally, we found that PEC surface expression of p55 dramatically decreased in the early stages of endotoxemia following intravenous LPS, while no change in p75 expression was detected. These data demonstrate a crucial in vivo role of p55 and an auxiliary role of p75 in TNF-mediated adhesion molecule upregulation on PECs. It is possible that the importance of the individual receptors varies at different stages of pulmonary microvascular inflammation following changes in their relative expression.


2021 ◽  
Author(s):  
Gilby Jepson ◽  
Barbara Carrapa ◽  
Jack Gillespie ◽  
Ran Feng ◽  
Peter DeCelles ◽  
...  

<p>Central Asia is one of the most tectonically active and orographically diverse regions in the world and is the location of the highest topography on Earth resulting from major plate tectonic collisional events. Yet the role of tectonics versus climate on erosion remains one of the greatest debates of our time. We present the first regional scale analysis of 2526 published low-temperature thermochronometric dates from Central Asia spanning the Altai-Sayan, Tian Shan, Tibet, Pamir, and Himalaya. We compare these dates to tectonic processes (proximity to tectonic boundaries, crustal thickness, seismicity) and state-of-the-art paleoclimate simulations in order to constrain the relative influences of climate and tectonics on the topographic architecture and erosion of Central Asia. Predominance of pre-Cenozoic ages in much of the interior of central Asia suggests that significant topography was created prior to the India-Eurasia collision and implies limited subsequent erosion. Increasingly young cooling ages are associated with increasing proximity to active tectonic boundaries, suggesting a first-order control of tectonics on erosion. However, areas that have been sheltered from significant precipitation for extensive periods of time retain old cooling ages. This suggests that ultimately climate is the great equalizer of erosion. Climate plays a key role by enhancing erosion in areas with developed topography and high precipitation such as the Tian Shan and Altai-Sayan during the Mesozoic and the Himalaya during the Cenozoic. Older thermochronometric dates are associated with sustained aridity following more humid periods.</p>


1983 ◽  
Vol 158 (4) ◽  
pp. 1077-1091 ◽  
Author(s):  
P Marrack ◽  
R Endres ◽  
R Shimonkevitz ◽  
A Zlotnik ◽  
D Dialynas ◽  
...  

We have examined the role of the murine homologue of Leu-3 T4, L3T4, in recognition of antigen in association with products of the major histocompatibility complex (Ag/MHC) by murine T cell hybridomas. A series of ovalbumin (OVA)/I-Ad-specific T cell hybridomas were ranked in their sensitivity to Ag/I by measuring their ability to respond to low doses of OVA, or their sensitivity to inhibition by anti-I-Ad antibodies. T cell hybridomas with low apparent avidity for OVA/I-Ad, i.e. that did not respond well to low concentrations of OVA and were easily inhibited by anti-I-Ad, were also easily inhibited by anti-L3T4 antibodies. The reverse was true for T cell hybridomas with apparent high avidity for Ag/MHC. We found that the presence of low doses of anti-L3T4 antibodies caused T cell hybridomas to respond less well to low doses of Ag, and to be more easily inhibited by anti-I-Ad antibodies. These results suggested that the role of the L3T4 molecule is to increase the overall avidity of the reaction between T cells and Ag-presenting cells. In support of this idea was the discovery of several L3T4- subclones of one of our L3T4+ T cell hybridomas, D0.11.10. The L3T4- subclones had the same amount of receptor for OVA/I-Ad as their L3T4+ parent, as detected by an anti-receptor monoclonal antibody. The L3T4- subclones, however, responded less well to low doses of OVA, and were more easily inhibited by anti-I-Ad antibodies than their L3T4/ parent. These results showed that the L3T4 molecule was not required for surface expression of, or functional activity of, the T cell receptor for Ag/MHC. The L3T4 molecule did, however, increase the sensitivity with which the T cell reacted with Ag/MHC on Ag-presenting cells.


Author(s):  
Yunkai Zhu ◽  
Fei Feng ◽  
Gaowei Hu ◽  
Yuyan Wang ◽  
Yin Yu ◽  
...  

SUMMARYThe global spread of SARS-CoV-2 is posing major public health challenges. One unique feature of SARS-CoV-2 spike protein is the insertion of multi-basic residues at the S1/S2 subunit cleavage site, the function of which remains uncertain. We found that the virus with intact spike (Sfull) preferentially enters cells via fusion at the plasma membrane, whereas a clone (Sdel) with deletion disrupting the multi-basic S1/S2 site instead utilizes a less efficient endosomal entry pathway. This idea was supported by the identification of a suite of endosomal entry factors specific to Sdel virus by a genome-wide CRISPR-Cas9 screen. A panel of host factors regulating the surface expression of ACE2 was identified for both viruses. Using a hamster model, animal-to-animal transmission with the Sdel virus was almost completely abrogated, unlike with Sfull. These findings highlight the critical role of the S1/S2 boundary of the SARS-CoV-2 spike protein in modulating virus entry and transmission.


Author(s):  
Raymond Rowland ◽  
Alberto Brandariz-Nuñez

Understanding the role of glycosylation in the virus-receptor interaction is important for developing approaches that disrupt infection. In this study, we showed that deglycosylation of both ACE2 and S had a minimal effect on the spike-ACE2 interaction.


Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 928-928
Author(s):  
Philip Murphy ◽  
Edel Mullen ◽  
Stephen Bergin ◽  
Geraldine Healy ◽  
Michelle Lavin ◽  
...  

Abstract Red Blood Cells from COVID-19 Patients Show Evidence of Increased Oxidative Stress and Increased Lactate Influx Corona Disease 19 (COVID-19) is caused by SARS-CoV-2, a novel, highly infectious, single stranded RNA virus. In severe cases, excess oxidative stress produced by a 'cytokine storm' may generate excess reactive oxygen species (ROS) and lead to tissue damage in the lungs and elsewhere. As the potential role of RBCs in the pathophysiology of COVID-19 remains controversial (1), we investigated for evidence of increased oxidative stress and increased thrombotic tendency in RBCs from patients with COVID-19 infection. Following ethical approval and written informed consent, we used flow cytometry (BD FACSCanto II) to measure baseline RBC ROS following incubation with 2'-7'-dichlorofluorescein diacetate (DCF). RBC ROS were also measured following pre-incubation with hydrogen peroxide (H2O2) (2mM) +/- antioxidant N-acetyl cysteine (NAC) (0.6mM). We also measured RBC surface expression of adhesion molecules CD44, CD47 and CD242, as well as CD147. Results were expressed as mean +/- standard deviation (SD). RBC ROS were measured in 22 COVID-19 positive patients and in 10 age matched healthy controls. One patient died from respiratory failure, whilst only 3 others required ITU admission for continuous positive airway pressure (CPAP) or intubation. There was no statistical difference in mean basal RBC DCF mean fluorescence intensity (MFI) levels between COVID-19 positive patients and controls. However, mean increase in RBC DCF MFI following H2O2 incubation was significantly higher in the COVID-19 positive group (1105.7+/-336.3) compared to the control group (843.4+/-256.7)( p= 0.042). The increase in RBC DCF MFI in the COVID-19 positive group correlated with CRP (p=0.014) but not with D-dimer, serum ferritin or any complete blood count (CBC) parameters. Incubation of RBC with 0.6 mM NAC for 30 minutes prior to H2O2 exposure caused a mean reduction in DCF MFI of 26.7% in the COVID-19 positive group. RBC expression of CD44, CD47, CD242 and CD147 were measured In a separate cohort of COVID-19 positive patients (n=32), and in 22 age matched controls. There were no statistically significant differences in mean expression levels of CD44, CD47 and CD242 between the 2 groups. However, mean RBC CD147 MFI expression was higher in the COVID-19 group (1319.64+/-374.76) compared to controls (1061.59+/-253.33) (p=0.018). There was no significant correlation between RBC CD147 MFI and D-dimer, CRP, serum ferritin or any CBC parameters in the COVID-19 positive group. However, 21 of the 32 COVID-19 positive patients had blood lactate levels measured and there was a positive correlation between CD147 MFI expression and blood lactate (R=0.56, p=0.0077). Induction of oxidative stress by H2O2 resulted in a greater increase in ROS in RBCs from COVID-19 patients compared to controls and with correlation to CRP, despite the fact that there were very few patients with severe disease in the study. This suggests a role for oxidative stress in disease pathogenesis. Pre-incubation with NAC attenuated this increase in ROS, suggesting a possible role for antioxidants in therapy. Increased RBC cell surface expression of adhesion molecules CD44, CD47 and CD242 can facilitate RBC interaction with platelets and/or endothelial cells, potentially contributing to thrombosis. We found no increase in their expression in COVID-19 patients compared to controls although RBCs may contribute to thrombosis in COVID-19 infection by other means (1). CD147 is tightly associated with and enables proper expression of monocarboxylate transporter 1, the lactate transporter for RBCs. We found increased surface expression of CD147 on RBCs of COVID-19 patients, whilst CD147 expression showed a moderate correlation with serum lactate levels, suggesting that RBCs in COVID-19 infection may be acting as a lactate sink to protect against lactic acidosis. In summary, our study suggests that COVID-19 infection causes increased oxidative stress and increased lactate influx in RBCs. Further studies are warranted into the role of RBCs in COVID-19 infection. Reference: (1) Murphy P, Glavey S, Quinn J. Anemia and red blood cell abnormalities in COVID-19. Leuk Lymphoma 2021;62:1539 Disclosures Quinn: Takeda: Honoraria. Glavey: Abbvie: Research Funding; Celgene and BMS company: Research Funding; Janssen: Honoraria, Research Funding; Amgen: Honoraria, Research Funding.


1998 ◽  
Vol 275 (5) ◽  
pp. C1239-C1246 ◽  
Author(s):  
Milagros Ferrer ◽  
Matilde S. Ayuso ◽  
Nora Butta ◽  
Roberto Parrilla ◽  
Consuelo González-Manchón

The platelet GPIIb-GPIIIa heterodimer (integrin αIIbβ3) binds fibrinogen with high affinity in response to activation by agonists, leading to platelet aggregation and formation of a hemostatic plug. The326GRV motif in GPIIb is highly conserved in the α-subunit of other integrins, suggesting that it might play an important functional role. Moreover, Arg327→His substitution in GPIIb has been associated with defective platelet surface expression of GPIIb-IIIa and thrombasthenic phenotype. This work aimed at elucidating whether the absence of Arg327or its substitution by His was responsible for the impaired surface expression of GPIIb-IIIa complexes. Transfection of cDNA encoding [Ala327]GPIIb, [Gln327]GPIIb, or [Phe327]GPIIb into Chinese hamster ovary cells inherently expressing GPIIIa permitted surface exposure of GPIIb-IIIa complexes, whereas [Glu327]GPIIb did not. These observations indicate that it is not the loss of [Arg327]GPIIb but the presence of His327or a negatively charged residue like Glu at position 327 of GPIIb that prevents the surface exposure of GPIIb-IIIa heterodimers. In contrast, changing Gln344, the homologue to Arg327in the α-subunit of the vitronectin receptor, to His did not prevent the surface expression of αv-GPIIIa complexes. Thus the conformational constraint imposed by His327seems to be rather specific for the heterodimerization and/or processing of GPIIb-IIIa complexes.


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