scholarly journals Biological Utilization and Regeneration of Silicon in Lake Michigan

1977 ◽  
Vol 34 (4) ◽  
pp. 537-544 ◽  
Author(s):  
H. L. Conway ◽  
J. I. Parker ◽  
E. M. Yaguchi ◽  
D. L. Mellinger
Keyword(s):  
Phytoplankton Community ◽  
Lake Michigan ◽  
Early Summer ◽  
Biologically Active ◽  
Soluble Form ◽  
Diatom Community ◽  
Southern Basin ◽  
Depth Profiles ◽  
Dissolved Silicon ◽  
Particulate Silicon

Depth profiles of dissolved reactive silicon and amorphous particulate silicon were made at monthly intervals (April–November 1975) at stations along a southwest transect from Grand Haven, Michigan, to a point approximately in the center of the southern basin of Lake Michigan Biological utilization of reactive silicon occurred prior to stratification in late May or early June. A shift from a 100% diatom-dominated phytoplankton community in spring to ~ 12% diatoms in August was attributed to the low dissolved silicon values observed in the surface water (< 2 μmol/ℓ) during summer. The total amount of biologically active silicon (TBAS) for the lake was found to be approximately 19 μmol/ℓ. Winter values were ~ 2 mol/ℓ amorphous silicon and ~ 17 μmol/ℓ reactive silicon. During the period June–August 80% of TBAS had been utilized by the diatom community, with only 20% remaining as reactive silicon. Greater than 50% of TBAS was lost from the water column during spring and early summer, which was attributed to settling of diatom frustules and the sinking of zooplankton fecal pellets containing frustules. This silicon was subsequently returned, in a soluble form, to the deep water during the fall. The amount of TBAS that was recycled was estimated to be 80–100%. Key words: Lake Michigan, diatoms, recycling, dissolution, limitation, silicon

scholarly journals Spatial and temporal distribution of phytoplankton in Lake Skadar

2012 ◽  
Vol 64 (2) ◽  
pp. 585-595 ◽  
Author(s):  
Jelena Rakocevic
Keyword(s):  
Spatial Heterogeneity ◽  
Phytoplankton Community ◽  
General Pattern ◽  
Seasonal Succession ◽  
Temporal Distribution ◽  
Late Summer ◽  
Early Summer ◽  
Quantitative Composition ◽  
Autumn And Winter ◽  
Lake Skadar

Phytoplankton seasonal succession and spatial heterogeneity were studied in Lake Skadar from February to December 2004. A total of 167 taxa from 6 algal divisions were observed, with Bacillariophyta being best represented (52.8%). The general pattern of phytoplankton seasonal succession in Lake Skadar was: Bacillariophyta in the spring, Chlorophyta in early summer, Cyanobacteria and Chlorophyta in late summer and Bacillariophyta and Chlorophyta in autumn and winter. Distinct spatial heterogeneity was observed. The central, open part of the lake (pelagic zone) was characterized by dominant euplanktonic species, mostly diatoms, whereas the western and northwestern parts (more isolated and shallower) had higher abundance of greens and blue-greens and a higher percentage of resuspended benthic-epiphytic forms in the phytoplankton community. Comparison with former phytoplankton data showed distinct differences in terms of the qualitative and quantitative composition of the phytoplankton community of Lake Skadar, which indicates lake deterioration.

Nutrient limitation of phytoplankton in the upper Swan River estuary, Western Australia

1996 ◽  
Vol 47 (4) ◽  
pp. 659 ◽  
Author(s):  
PA Thompson ◽  
W Hosja
Keyword(s):  
Nutrient Limitation ◽  
Chlorophyll A ◽  
Phytoplankton Community ◽  
River Estuary ◽  
Early Summer ◽  
Phosphate Silicate ◽  
Cell Densities ◽  
And Control ◽  
Swan River ◽  
Second Peak

During 1993-94 the phytoplankton community in the upper Swan River estuary had a peak chlorophyll a concentration of 57 mg m-3 during early summer (December 1993) and a second peak of 35 mg m-3 during late autumn (May 1994). Mid summer was characterized by low cell densities and low chlorophyll a concentrations. The potential of the phytoplankton community for nutrient limitation was assessed with dilution bioassays given nutrient mixes deficient in one of the following: nitrogen, phosphate, silicate, iron, trace metals, chelators, or vitamins. During the mid-summer period of low phytoplankton abundance, nitrogen was the nutrient with the greatest potential to limit algal biomass. During mid summer, ambient N:P ratios tended to be near unity and bioassays indicated that the available pool of N was up to 20 times more limiting to biomass development than was available P. Also during mid summer, bioassay treatments given no nitrogen and control treatments given no nutrients showed little growth, reaching chlorophyll a concentrations -1/30th of those given a full suite of nutrients. Chlorophyll a concentrations in the bioassay control treatments given no nutrients were correlated (r2 = 0.74) with measured surface nitrate concentrations; this suggested that nitrate inputs may be a major factor controlling phytoplankton biomass in this ecosystem. The correlation between surface nitrate concentration and rainfall (r2 = 0.69) further suggests that rainfall may be the most important mechanism supplying nitrate to the surface waters of this estuary.

scholarly journals Antiviral Treatment with Alpha Interferon Up-Regulates CD14 on Liver Macrophages and Its Soluble Form in Patients with Chronic Hepatitis B

2005 ◽  
Vol 49 (2) ◽  
pp. 590-599 ◽  
Author(s):  
Patrizia Carotenuto ◽  
Debby van Riel ◽  
André Artsen ◽  
Sven Bruijns ◽  
Fons G. Uytdehaag ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Antiviral Treatment ◽  
Biologically Active ◽  
Alpha Interferon ◽  
Regulatory Function ◽  
Soluble Form

ABSTRACT To investigate whether therapy with alpha interferon (IFN-α) induces changes in intrahepatic antigen-presenting cells (APCs), we obtained liver biopsy specimens before, during, and after therapy with IFN-α from chronic hepatitis B patients whose viral load had already been reduced by at least 8 weeks of treatment with lamivudine. HLA-DR, CD1a, and CD83 were not modified by the therapy. The intralobular expression of CD68 on Kupffer cells remained stable, denoting no changes in the number of resident macrophages during IFN-α treatment. In contrast, CD14 was weakly expressed in the absence of IFN-α and was significantly up-regulated during therapy. At the same time, the levels of soluble CD14 and interleukin-10 in plasma increased significantly. In vitro, monocytes maintained in the presence of IFN-α differentiated into macrophages or dendritic cells with higher levels of expression of CD14 than that for the control cultures. During therapy with IFN-α, T-cell infiltration in the portal spaces was reduced, mainly due to a significant decrease in the number of CD8+ T cells. These findings show that IFN-α is biologically active on APCs in vivo and in vitro and suggest that this newly described regulatory function, together with the already known inhibitory effects on lymphocytes, may cooperate to reduce inflammation and consequent tissue damage in patients with chronic viral hepatitis.

scholarly journals Pref-1 Interacts with Fibronectin To Inhibit Adipocyte Differentiation

2010 ◽  
Vol 30 (14) ◽  
pp. 3480-3492 ◽  
Author(s):  
Yuhui Wang ◽  
Ling Zhao ◽  
Cynthia Smas ◽  
Hei Sook Sul
Keyword(s):  
Adipocyte Differentiation ◽  
Transmembrane Protein ◽  
Dominant Negative ◽  
Biologically Active ◽  
Mitogen Activated Protein Kinase ◽  
Soluble Form ◽  
Necrosis Factor Alpha ◽  
Rgd Peptides ◽  
Downstream Signaling ◽  
Erk Mapk

ABSTRACT Pref-1/Dlk1 is made as an epidermal growth factor (EGF) repeat-containing transmembrane protein but is cleaved by tumor necrosis factor alpha converting enzyme (TACE) to generate a biologically active soluble form. Soluble Pref-1 inhibits adipocyte differentiation through the activation of extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) and the subsequent upregulation of Sox9 expression. However, others have implicated Notch in Pref-1 signaling and function. Here, we show that Pref-1 does not interact with, or require, Notch for its function. Instead, we show a direct interaction of Pref-1 and fibronectin via the Pref-1 juxtamembrane domain and fibronectin C-terminal domain. We also show that fibronectin is required for the Pref-1-mediated inhibition of adipocyte differentiation, the activation of ERK/MAPK, and the upregulation of Sox9. Furthermore, disrupting fibronectin binding to integrin by the addition of RGD peptides or by the knockdown of α5 integrin prevents the Pref-1 inhibition of adipocyte differentiation. Pref-1 activates the integrin downstream signaling molecules, FAK and Rac, and ERK activation by Pref-1 is blunted by the knockdown of Rac or by the forced expression of dominant-negative Rac. We conclude that, by interacting with fibronectin, Pref-1 activates integrin downstream signaling to activate MEK/ERK and to inhibit adipocyte differentiation.

scholarly journals Pref-1 (Preadipocyte Factor 1) Activates the MEK/Extracellular Signal-Regulated Kinase Pathway To Inhibit Adipocyte Differentiation

2006 ◽  
Vol 27 (6) ◽  
pp. 2294-2308 ◽  
Author(s):  
Kyung-Ah Kim ◽  
Jung-Hyun Kim ◽  
Yuhui Wang ◽  
Hei Sook Sul
Keyword(s):  
Adipocyte Differentiation ◽  
Transmembrane Protein ◽  
Biologically Active ◽  
Soluble Form ◽  
Null Mouse ◽  
Dependent Manner ◽  
Wild Type ◽  
Extracellular Signal Regulated Kinase ◽  
Erk Phosphorylation ◽  
Extracellular Signal

ABSTRACT Preadipocyte factor 1 (Pref-1) is found in preadipocytes but is absent in adipocytes. Pref-1 is made as a transmembrane protein but is cleaved to generate a biologically active soluble form. Although Pref-1 inhibition of adipogenesis has been well studied in vitro and in vivo, the signaling pathway for Pref-1 is not known. Here, by using purified soluble Pref-1 in Pref-1 null mouse embryo fibroblasts (MEF), we show that Pref-1 increases MEK/extracellular signal-regulated kinase (ERK) phosphorylation in a time- and dose-dependent manner. Compared to wild-type MEF, differentiation of Pref-1 null MEF into adipocytes is enhanced, as judged by lipid accumulation and adipocyte marker expression. Both wild-type and Pref-1 null MEF show a transient burst of ERK phosphorylation upon addition of adipogenic agents. Wild-type MEF show a significant, albeit lower, second increase in ERK phosphorylation peaking at day 2. This ERK phosphorylation, corresponding to Pref-1 abundance, is absent during differentiation of Pref-1 null MEF. Prevention of this second increase in ERK1/2 phosphorylation in wild-type MEF by the MEK inhibitor PD98059 or by transient depletion of ERK1/2 via small interfering RNA-enhanced adipocyte differentiation. Furthermore, treatment of Pref-1 null MEF with Pref-1 restores this ERK phosphorylation, resulting in inhibition of adipocyte differentiation primarily by preventing peroxisome proliferator-activated receptor γ2 induction. However, in the presence of PD98059 or depletion of ERK1/2, exogenous Pref-1 cannot inhibit adipocyte differentiation in Pref-1 null MEF. We conclude that Pref-1 activates MEK/ERK signaling, which is required for Pref-1 inhibition of adipogenesis.

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