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  • 1
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    Seawater carbonate chemistry and ecosystem calcification, community production of coral reef (2017)
    PANGAEA
    In:  Supplement to: DeCarlo, Thomas M; Cohen, Anne L; Wong, George T F; Shiah, Fuh Kwo; Lentz, S J; Davis, Kristen A; Shamberger, K E F; Lohmann, Pat (2017): Community production modulates coral reef pH and the sensitivity of ecosystem calcification to ocean acidification. Journal of Geophysical Research: Oceans, 122, 745–761, https://doi.org/10.1002/2016JC012326
    Details
    Publication Date: 2024-03-15
    Description: Coral reefs are built of calcium carbonate (CaCO3) produced biogenically by a diversity of calcifying plants, animals and microbes. As the ocean warms and acidifies, there is mounting concern that declining calcification rates could shift coral reef CaCO3 budgets from net accretion to net dissolution. We quantified net ecosystem calcification (NEC) and production (NEP) on Dongsha Atoll, northern South China Sea, over a two-week period that included a transient bleaching event. Peak daytime pH on the wide, shallow reef flat during the non-bleaching period was 8.5, significantly elevated above that of the surrounding open ocean (8.0-8.1) as a consequence of daytime NEP (up to 112 mmol C/m**2/h). Diurnal-averaged NEC was 390?+/-?90 mmol CaCO3/m**2/day, higher than any other coral reef studied to date despite comparable calcifier cover (25%) and relatively high fleshy algal cover (19%). Coral bleaching linked to elevated temperatures significantly reduced daytime NEP by 29 mmol C/m**2/h. pH on the reef flat declined by 0.2 units, causing a 40% reduction in NEC in the absence of pH changes in the surrounding open ocean. Our findings highlight the interactive relationship between carbonate chemistry of coral reef ecosystems and ecosystem production and calcification rates, which are in turn impacted by ocean warming. As open-ocean waters bathing coral reefs warm and acidify over the 21st century, the health and composition of reef benthic communities will play a major role in determining on-reef conditions that will in turn dictate the ecosystem response to climate change.
    Keywords: Alkalinity, total; Aragonite saturation state; Benthos; Bicarbonate ion; Calcification/Dissolution; Calcification rate, standard deviation; Calcite saturation state; Calculated using seacarb after Nisumaa et al. (2010); Carbon, inorganic, dissolved; Carbon, net production; Carbonate ion; Carbonate system computation flag; Carbon dioxide; Carbon dioxide, air-sea, flux; Coast and continental shelf; Density; DEPTH, water; Dongsha_Atoll; Entire community; EXP; Experiment; Field observation; Fugacity of carbon dioxide (water) at sea surface temperature (wet air); Irradiance; Net calcification rate of calcium carbonate; Net community production, carbon dioxide, standard deviation; North Pacific; OA-ICC; Ocean Acidification International Coordination Centre; Partial pressure of carbon dioxide (water) at sea surface temperature (wet air); pH; Primary production/Photosynthesis; Rocky-shore community; Salinity; Sampling date; Temperature, water; Time, standard deviation; Time in hours; Tropical; Type
    Type: Dataset
    Format: text/tab-separated-values, 1440 data points
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    DATA PANGAEA
  • 2
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    Diverse coral communities in naturally acidified waters of a Western Pacific reef (2014)
    PANGAEA
    In:  Supplement to: Shamberger, K E F; Cohen, Anne L; Golbuu, Yimnang; McCorkle, Daniel C; Lentz, S J; Barkley, Hannah C (2014): Diverse coral communities in naturally acidified waters of a Western Pacific reef. Geophysical Research Letters, 41(2), 499-504, https://doi.org/10.1002/2013GL058489
    Details
    Publication Date: 2024-03-15
    Description: Anthropogenic carbon dioxide emissions are acidifying the oceans, reducing the concentration of carbonate ions ([CO32-) that calcifying organisms need to build and cement coral reefs. To date, studies of a handful of naturally acidified reef systems reveal depauperate communities, sometimes with reduced coral cover and calcification rates, consistent with results of laboratory-based studies. Here we report the existence of highly diverse, coral-dominated reef communities under chronically low pH and aragonite saturation state (Omega ar). Biological and hydrographic processes change the chemistry of the seawater moving across the barrier reefs and into Palau's Rock Island bays, where levels of acidification approach those projected for the western tropical Pacific open ocean by 2100. Nevertheless, coral diversity, cover, and calcification rates are maintained across this natural acidification gradient. Identifying the combination of biological and environmental factors that enable these communities to persist could provide important insights into the future of coral reefs under anthropogenic acidification.
    Keywords: Alkalinity, total; Aragonite saturation state; Aragonite saturation state, standard error; Benthos; Bicarbonate ion; Calcite saturation state; Calculated using CO2SYS; Calculated using seacarb after Nisumaa et al. (2010); Carbon, inorganic, dissolved; Carbonate ion; Carbonate system computation flag; Carbon dioxide; Coast and continental shelf; Community composition and diversity; Coulometric titration; Coverage; Coverage, standard error; Diversity; Diversity, standard error; Entire community; EXP; Experiment; Field observation; Fugacity of carbon dioxide (water) at sea surface temperature (wet air); North Pacific; OA-ICC; Ocean Acidification International Coordination Centre; Palauan_reef; Partial pressure of carbon dioxide (water) at sea surface temperature (wet air); pH; Potentiometric titration; Rocky-shore community; Salinity; Site; Species richness; Species richness, standard error; Temperature, water; Tropical
    Type: Dataset
    Format: text/tab-separated-values, 132 data points
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    DATA PANGAEA
  • 3
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    Genomic characterization of the Bacillus cereus sensu lato species: Backdrop to the evolution of Bacillus anthracis [RESEARCH] (2012)
    Cold Spring Harbor Laboratory Press
    Details
    Publication Date: 2012-08-02
    Description: The key genes required for Bacillus anthracis to cause anthrax have been acquired recently by horizontal gene transfer. To understand the genetic background for the evolution of B. anthracis virulence, we obtained high-redundancy genome sequences of 45 strains of the Bacillus cereus sensu lato (s.l.) species that were chosen for their genetic diversity within the species based on the existing multilocus sequence typing scheme. From the resulting data, we called more than 324,000 new genes representing more than 12,333 new gene families for this group. The core genome size for the B. cereus s.l. group was ~1750 genes, with another 2150 genes found in almost every genome constituting the extended core. There was a paucity of genes specific and conserved in any clade. We found no evidence of recent large-scale gene loss in B. anthracis or for unusual accumulation of nonsynonymous DNA substitutions in the chromosome; however, several B. cereus genomes isolated from soil and not previously associated with human disease were degraded to various degrees. Although B. anthracis has undergone an ecological shift within the species, its chromosome does not appear to be exceptional on a macroscopic scale compared with close relatives.
    Electronic ISSN: 1549-5469
    Topics: Biology , Medicine
    Published by Cold Spring Harbor Laboratory Press
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  • 4
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    Genetic Ablation of Extra Domain A of Fibronectin in Hypercholesterolemic Mice Improves Stroke Outcome by Reducing Thrombo-Inflammation [Vascular Medicine] (2015)
    American Heart Association (AHA)
    Details
    Publication Date: 2015-12-08
    Description: Background— The fibronectin-splicing variant containing extra domain A (Fn-EDA) is present in negligible amounts in the plasma of healthy humans but markedly elevated in patients with comorbid conditions, including diabetes mellitus and hypercholesterolemia, which are risk factors for stroke. It remains unknown, however, whether Fn-EDA worsens stroke outcomes in such conditions. We determined the role of Fn-EDA in stroke outcome in a model of hypercholesterolemia, the apolipoprotein E–deficient (Apoe –/– ) mouse. Methods and Results— In a transient cerebral ischemia/reperfusion injury model, Apoe –/– mice expressing fibronectin deficient in EDA (Fn-EDA –/– Apoe –/– mice) exhibited smaller infarcts and improved neurological outcomes at days 1 and 8 ( P 〈0.05 versus Apoe –/– mice). Concomitantly, intracerebral thrombosis [assessed by fibrin(ogen) deposition] and postischemic inflammation (phospho–nuclear factor-B p65, phospho–IB kinase α/β, interleukin 1β, and tumor necrosis factor-α) within lesions of Fn-EDA –/– Apoe –/– mice were markedly decreased ( P 〈0.05 versus Apoe –/– mice). In an FeCl 3 injury–induced carotid artery thrombosis model, thrombus growth rate and the time to occlusion were prolonged in Fn-EDA –/– Apoe –/– mice ( P 〈0.05 versus Apoe –/– mice). Genetic ablation of TLR4 improved stroke outcome in Apoe –/– mice ( P 〈0.05) but had no effect on stroke outcome in Fn-EDA –/– Apoe –/– mice. Bone marrow transplantation experiments revealed that nonhematopoietic cell–derived Fn-EDA exacerbates stroke through Toll-like receptor-4 expressed on hematopoietic cells. Infusion of a specific inhibitor of Fn-EDA into Apoe –/– mouse 15 minutes after reperfusion significantly improved stroke outcome. Conclusions— Hypercholesterolemic mice deficient in Fn-EDA exhibit reduced cerebral thrombosis and less inflammatory response after ischemia/reperfusion injury. These findings suggest that targeting Fn-EDA could be an effective therapeutic strategy in stroke associated with hypercholesterolemia.
    Keywords: Ischemic Stroke, Thrombosis
    Electronic ISSN: 1524-4539
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 5
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    Clinical and laboratory variability in a cohort of patients diagnosed with type 1 VWD in the United States (2016)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2016-05-20
    Description: von Willebrand disease (VWD) is the most common inherited bleeding disorder, and type 1 VWD is the most common VWD variant. Despite its frequency, diagnosis of type 1 VWD remains the subject of debate. In order to study the spectrum of type 1 VWD in the United States, the Zimmerman Program enrolled 482 subjects with a previous diagnosis of type 1 VWD without stringent laboratory diagnostic criteria. von Willebrand factor (VWF) laboratory testing and full-length VWF gene sequencing was performed for all index cases and healthy control subjects in a central laboratory. Bleeding phenotype was characterized using the International Society on Thrombosis and Haemostasis bleeding assessment tool. At study entry, 64% of subjects had VWF antigen (VWF:Ag) or VWF ristocetin cofactor activity below the lower limit of normal, whereas 36% had normal VWF levels. VWF sequence variations were most frequent in subjects with VWF:Ag 〈30 IU/dL (82%), whereas subjects with type 1 VWD and VWF:Ag ≥30 IU/dL had an intermediate frequency of variants (44%). Subjects whose VWF testing was normal at study entry had a similar rate of sequence variations as the healthy controls (14%). All subjects with severe type 1 VWD and VWF:Ag ≤5 IU/dL had an abnormal bleeding score (BS), but otherwise BS did not correlate with VWF:Ag. Subjects with a historical diagnosis of type 1 VWD had similar rates of abnormal BS compared with subjects with low VWF levels at study entry. Type 1 VWD in the United States is highly variable, and bleeding symptoms are frequent in this population.
    Keywords: Thrombosis and Hemostasis
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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  • 6
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    Antiphospholipid antibodies and recurrent thrombosis after a first unprovoked venous thromboembolism (2018)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2018-05-11
    Description: It is uncertain whether antiphospholipid antibodies (APAs) increase the risk of recurrence after a first unprovoked venous thromboembolism (VTE). We tested for anticardiolipin antibodies, anti–β2 glycoprotein 1 antibodies, and lupus anticoagulant on 2 occasions ~6 months apart in 307 patients with a first unprovoked VTE who were part of a prospective cohort study. We then determined if APAs were associated with recurrent thrombosis in the 290 patients who stopped anticoagulant therapy in response to negative D-dimer results. Compared with those without an APA, the hazard ratios for recurrent VTE were 1.8 (95% confidence interval [CI], 0.9-3.7; P = .09) in the 25.9% of patients with an APA on ≥1 occasions, 2.7 (95% CI, 1.1-.7; P = .03) in the 9.0% of patients with the same APA on 2 occasions, and 4.5 (95% CI, 1.5-13.0; P = .006) in the 3.8% of patients with 2 or 3 different APA types on either the same or different occasions. There was no association between having an APA and D-dimer levels. We conclude that having the same type of APA on 2 occasions or having 〉1 type of APA on the same or different occasions is associated with recurrent thrombosis in patients with a first unprovoked VTE who stop anticoagulant therapy in response to negative D-dimer tests. APA and D-dimer levels seem to be independent predictors of recurrence in patients with an unprovoked VTE. This trial was registered at www.clinicaltrials.gov as #NCT00720915.
    Keywords: Thrombosis and Hemostasis, Clinical Trials and Observations
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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  • 7
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    Dominant negative PPAR{gamma} promotes atherosclerosis, vascular dysfunction, and hypertension through distinct effects in endothelium and vascular muscle (2013)
    The American Physiological Society (APS)
    Details
    Publication Date: 2013-05-02
    Description: Agonists of the nuclear hormone receptor peroxisome proliferator-activated receptor (PPAR) have potent insulin-sensitizing effects and inhibit atherosclerosis progression in patients with Type II diabetes. Conversely, missense mutations in the ligand-binding domain of PPAR that render the transcription factor dominant negative (DN) cause early-onset hypertension and Type II diabetes. We tested the hypothesis that DN PPAR-mediated interference of endogenous wild-type PPAR in the endothelium and vascular smooth muscle exacerbates atherosclerosis in apolipoprotein E-deficient (ApoE –/– ) mice. Endothelium-specific expression of DN PPAR on the ApoE –/– background unmasked significant impairment of endothelium-dependent relaxation in aortic rings, increased systolic blood pressure, altered expression of atherogenic markers (e.g., Cd36 , Mcp1 , Catalase ), and enhanced diet-induced atherosclerotic lesion formation in aorta. Smooth muscle-specific expression of DN PPAR, which induces aortic dysfunction and increased systolic blood pressure at baseline, also resulted in enhanced diet-induced atherosclerotic lesion formation in aorta on the ApoE –/– background that was associated with altered expression of a shared, yet distinct, set of atherogenic markers (e.g., Cd36 , Mcp1 , Osteopontin , Vcam1 ). In particular, induction of Osteopontin expression by smooth muscle-specific DN PPAR correlated with increased plaque calcification. These data demonstrate that inhibition of PPAR function specifically in the vascular endothelium or smooth muscle may contribute to cardiovascular disease.
    Print ISSN: 0363-6119
    Electronic ISSN: 1522-1490
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 8
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    ADAMTS13 reduces vascular inflammation and the development of early atherosclerosis in mice (2012)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2012-03-09
    Description: ADAMTS13, a metalloprotease, plays a pivotal role in preventing spontaneous microvascular thrombosis by cleaving hyperactive ultra large von Willebrand factor multimers into smaller, less active multimers. Reduced ADAMTS13 activity in plasma has been described in many diseases associated with systemic inflammation. It remains uncertain, however, whether ADAMTS13 contributes to disease pathogenesis or rather simply serves as an inflammation-associated marker. We hypothesized that, by decreasing vascular inflammation, ADAMTS13 reduces the development of early atherosclerotic plaques. Using intravital fluorescence microscopy, we observed excessive leukocyte adhesion and accelerated atherosclerotic plaque formation at the carotid sinus of Adamts13 –/– /ApoE –/– mice compared with ApoE –/– mice fed a high-fat Western diet. At 4 months of age, there was a significant increase in atherosclerosis in the aorta and aortic sinus of Adamts13 –/– /ApoE –/– mice compared with ApoE –/– mice. Interestingly, we detected a 2-fold increase in macrophage recruitment to the atherosclerotic plaque of the Adamts13 –/– /ApoE –/– mice compared with ApoE –/– mice, suggesting that the atherosclerotic lesions in these mice were not only larger but also more inflammatory. These findings reveal a new functional role for the antithrombotic enzyme ADAMTS13 in reducing excessive vascular inflammation and plaque formation during early atherosclerosis.
    Keywords: Thrombosis and Hemostasis
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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  • 9
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    Paradoxical absence of a prothrombotic phenotype in a mouse model of severe hyperhomocysteinemia (2012)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2012-03-30
    Description: Hyperhomocysteinemia confers a high risk for thrombotic vascular events, but homocysteine-lowering therapies have been ineffective in reducing the incidence of secondary vascular outcomes, raising questions regarding the role of homocysteine as a mediator of cardiovascular disease. Therefore, to determine the contribution of elevated homocysteine to thrombosis susceptibility, we studied Cbs –/– mice conditionally expressing a zinc-inducible mutated human CBS (I278T) transgene. Tg-I278T Cbs –/– mice exhibited severe hyperhomocysteinemia and endothelial dysfunction in cerebral arterioles. Surprisingly, however, these mice did not display increased susceptibility to arterial or venous thrombosis as measured by photochemical injury in the carotid artery, chemical injury in the carotid artery or mesenteric arterioles, or ligation of the inferior vena cava. A survey of hemostatic and hemodynamic parameters revealed no detectible differences between control and Tg-I278T Cbs –/– mice. Our data demonstrate that severe elevation in homocysteine leads to the development of vascular endothelial dysfunction but is not sufficient to promote thrombosis. These findings may provide insights into the failure of homocysteine-lowering trials in secondary prevention from thrombotic vascular events.
    Keywords: Thrombosis and Hemostasis
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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  • 10
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    Vulnerability of the retinal microvasculature to oxidative stress: ion channel-dependent mechanisms (2012)
    The American Physiological Society (APS)
    Details
    Publication Date: 2012-05-02
    Description: Although oxidative stress is a hallmark of important vascular disorders such as diabetic retinopathy, it remains unclear why the retinal microvasculature is particularly vulnerable to this pathophysiological condition. We postulated that redox-sensitive ion channels may play a role. Using H 2 O 2 to cause oxidative stress in microvascular complexes freshly isolated from the adult rat retina, we assessed ionic currents, cell viability, intracellular oxidants, and cell calcium by using perforated-patch recordings, trypan blue dye exclusion, and fura-2 fluorescence, respectively. Supporting a role for the oxidant-sensitive ATP-sensitive K (K ATP ) channels, we found that these channels are activated during exposure of retinal microvessels to H 2 O 2 . Furthermore, their inhibition by glibenclamide significantly lessened H 2 O 2 -induced microvascular cell death. Additional experiments established that by increasing the influx of calcium into microvascular cells, the K ATP channel-mediated hyperpolarization boosted the vulnerability of these cells to oxidative stress. In addition to the K ATP channel-dependent mechanism for increasing the lethality of oxidative stress, we also found that the vulnerability of cells in the capillaries, but not in the arterioles, was further boosted by a K ATP channel-independent mechanism, which our experiments indicated involves the oxidant-induced activation of calcium-permeable nonspecific cation channels. Taken together, our findings support a working model in which both K ATP channel-independent and K ATP channel-dependent mechanisms render the capillaries of the retina particularly vulnerable to oxidative stress. Identification of these previously unappreciated mechanisms for boosting the lethality of oxidants may provide new targets for pharmacologically limiting damage to the retinal microvasculature during periods of oxidative stress.
    Print ISSN: 0363-6143
    Electronic ISSN: 1522-1563
    Topics: Medicine
    Published by The American Physiological Society (APS)
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