THE ROLE OF CONSECUTIVE BATCH CULTURE IN RUMEN MICROBIOLOGY

1984 ◽  
Vol 64 (5) ◽  
pp. 47-48 ◽  
Author(s):  
M. K. THEODOROU ◽  
D. J. GASCOYNE ◽  
D. E. BEEVER
Keyword(s):  
Steady State ◽  
Microbial Communities ◽  
Microbial Ecology ◽  
Key Words ◽  
Batch Culture ◽  
Rumen Fluid ◽  
Quasi Steady State ◽  
Batch Cultures

Anaerobic, forage-containing medium was inoculated with rumen fluid and consecutive batch cultures were established. Microbial communities were maintained and cultures demonstrated quasi-steady-state. The VFA proportions from consecutive batch cultures which were transferred at 3-day intervals were similar to those obtained in vivo. Key words: Microbial ecology, rumen, batch culture

scholarly journals Bacteriocin-like activity of oral Fusobacterium nucleatum isolated from human and non-human primates

1999 ◽  
Vol 30 (4) ◽  
pp. 324-346 ◽  
Author(s):  
Elerson Gaetti-Jardim Júnior ◽  
Mario Julio Avila-Campos
Keyword(s):  
Oral Cavity ◽  
Microbial Ecology ◽  
Dental Plaque ◽  
Fusobacterium Nucleatum ◽  
Antagonistic Activity ◽  
Healthy Individuals ◽  
Bacterial Microbiota ◽  
Reference Strains

Fusobacterium nucleatum is indigenous of the human oral cavity and has been involved in different infectious processes. The production of bacteriocin-like substances may be important in regulation of bacterial microbiota in oral cavity. The ability to produce bacteriocin-like substances by 80 oral F. nucleatum isolates obtained from periodontal patients, healthy individuals and Cebus apella monkeys, was examinated. 17.5% of all tested isolates showed auto-antagonism and 78.8% iso- or hetero-antagonism. No isolate from monkey was capable to produce auto-inhibition. In this study, the antagonistic substances production was variable in all tested isolates. Most of the F. nucleatum showed antagonistic activity against tested reference strains. These data suggest a possible participation of these substances on the oral microbial ecology in humans and animals. However, the role of bacteriocins in regulating dental plaque microbiota in vivo is discussed.

DPP10 is an inactivation modulatory protein of Kv4.3 and Kv1.4

2006 ◽  
Vol 291 (5) ◽  
pp. C966-C976 ◽  
Author(s):  
Hong-Ling Li ◽  
Yu-Jie Qu ◽  
Yi Chun Lu ◽  
Vladimir E. Bondarenko ◽  
Shimin Wang ◽  
...  
Keyword(s):  
Steady State ◽  
Interacting Protein ◽  
Voltage Gated ◽  
Time To Peak ◽  
Kv Channel ◽  
Closed State ◽  
Channel Inactivation ◽  
Recovery From Inactivation

Voltage-gated K+ channels exist in vivo as multiprotein complexes made up of pore-forming and ancillary subunits. To further our understanding of the role of a dipeptidyl peptidase-related ancillary subunit, DPP10, we expressed it with Kv4.3 and Kv1.4, two channels responsible for fast-inactivating K+ currents. Previously, DPP10 has been shown to effect Kv4 channels. However, Kv1.4, when expressed with DPP10, showed many of the same effects as Kv4.3, such as faster time to peak current and negative shifts in the half-inactivation potential of steady-state activation and inactivation. The exception was recovery from inactivation, which is slowed by DPP10. DPP10 expressed with Kv4.3 caused negative shifts in both steady-state activation and inactivation of Kv4.3, but no significant shifts were detected when DPP10 was expressed with Kv4.3 + KChIP2b (Kv channel interacting protein). DPP10 and KChIP2b had different effects on closed-state inactivation. At −60 mV, KChIP2b nearly abolishes closed-state inactivation in Kv4.3, whereas it developed to a much greater extent in the presence of DPP10. Finally, expression of a DPP10 mutant consisting of its transmembrane and cytoplasmic 58 amino acids resulted in effects on Kv4.3 gating that were nearly identical to those of wild-type DPP10. These data show that DPP10 and KChIP2b both modulate Kv4.3 inactivation but that their primary effects are on different inactivation states. Thus DPP10 may be a general modulator of voltage-gated K+ channel inactivation; understanding its mechanism of action may lead to deeper understanding of the inactivation of a broad range of K+ channels.

scholarly journals Optogenetic Tools for Control of Public Goods in Saccharomyces cerevisiae

mSphere ◽  
2021 ◽  
Vol 6 (4) ◽  
Author(s):  
Neydis Moreno Morales ◽  
Michael T. Patel ◽  
Cameron J. Stewart ◽  
Kieran Sweeney ◽  
Megan N. McClean
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Community Development ◽  
Public Goods ◽  
Microbial Communities ◽  
Microbial Ecology ◽  
Intercellular Interactions ◽  
Recent Advances

Recent advances in microbial ecology have highlighted the importance of intercellular interactions in controlling the development, composition, and resilience of microbial communities. In order to better understand the role of these interactions in governing community development, it is critical to be able to alter them in a controlled manner.

BODY ORGAN CYTOCHROME OXIDASE ACTIVITY IN COLD- AND WARM-ACCLIMATED RATS

1963 ◽  
Vol 41 (9) ◽  
pp. 1847-1854 ◽  
Author(s):  
Ladislav Janský
Keyword(s):  
Steady State ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Whole Body ◽  
Cytochrome Oxidase Activity ◽  
Full Capacity ◽  
Body Organ ◽  
Total Body

The cytochrome oxidase activity was estimated in homogenates of the whole body and in nine body organs of cold- and warm-acclimated rats. The total body cytochrome oxidase activity expressed in terms of oxygen consumption was similar in cold- and warm-acclimated rats. In cold-acclimated animals the total cytochrome oxidase activity did not differ from maximal steady state metabolism measured in vivo, while in warm-acclimated rats the total cytochrome oxidase activity was almost twice as great as the maximal steady state metabolism. The results indicate that warm-acclimated rats do not utilize the full capacity of the cytochrome system and that cold-acclimation makes full exploitation of the oxidase capacity possible. In cold-acclimated rats the cytochrome oxidase activity of the muscles comprised 57% of the total, the liver 22.5%, and the skin 6%, with smaller roles for other organs. The role of the liver was greater in cold-acclimated than in warm-acclimated rats.

scholarly journals Microbial communities in a dynamic in vitro model for the human ileum resemble the human ileal microbiota

2019 ◽  
Vol 95 (8) ◽  
Author(s):  
Maria Stolaki ◽  
Mans Minekus ◽  
Koen Venema ◽  
Leo Lahti ◽  
Eddy J Smid ◽  
...  
Keyword(s):  
Steady State ◽  
Microbial Communities ◽  
In Vitro Model ◽  
Phylogenetic Profiles ◽  
Two Samples ◽  
Microbial Stability ◽  
Vitro Model ◽  
And Cluster Analysis

ABSTRACT The important role for the human small intestinal microbiota in health and disease has been widely acknowledged. However, the difficulties encountered in accessing the small intestine in a non-invasive way in healthy subjects have limited the possibilities to study its microbiota. In this study, a dynamic in vitro model that simulates the human ileum was developed, including its microbiota. Ileostomy effluent and fecal inocula were employed to cultivate microbial communities within the in vitro model. Microbial stability was repetitively achieved after 10 days of model operation with bacterial concentrations reaching on average 107 to 108 16S rRNA copy numbers/ml. High diversities similar to those observed in in vivo ileum samples were achieved at steady state using both fecal and ileostomy effluent inocula. Functional stability based on Short Chain Fatty Acid concentrations was reached after 10 days of operation using fecal inocula, but was not reached with ileostomy effluent as inoculum. Principal Components and cluster analysis of the phylogenetic profiles revealed that in vitro samples at steady state clustered closest to two samples obtained from the terminal ileum of healthy individuals, independent of the inoculum used, demonstrating that the in vitro microbiota at steady state resembles that of the human ileum.

scholarly journals Regulation of steady-state neutrophil homeostasis by macrophages

Blood ◽  
2011 ◽  
Vol 117 (2) ◽  
pp. 618-629 ◽  
Author(s):  
Claire Gordy ◽  
Heather Pua ◽  
Gregory D. Sempowski ◽  
You-Wen He
Keyword(s):  
Steady State ◽  
Protein C ◽  
Marginal Zone ◽  
Extramedullary Hematopoiesis ◽  
Granulocyte Colony Stimulating Factor ◽  
Inhibitory Protein ◽  
Stimulating Factor ◽  
Defective Clearance

Abstract The timely clearance of apoptotic neutrophils from inflammation sites is an important function of macrophages; however, the role of macrophages in maintaining neutrophil homeostasis under steady-state conditions is less well understood. By conditionally deleting the antiapoptotic gene cellular FLICE-like inhibitory protein (C-FLIP) in myeloid cells, we have generated a novel mouse model deficient in marginal zone and bone marrow stromal macrophages. These mice develop severe neutrophilia, splenomegaly, extramedullary hematopoiesis, decreased body weight, and increased production of granulocyte colony-stimulating factor (G-CSF) and IL-1β, but not IL-17. c-FLIPf/f LysM-Cre mice exhibit delayed clearance of circulating neutrophils, suggesting that failure of macrophages to efficiently clear apoptotic neutrophils causes production of cytokines that drive excess granulopoiesis. Further, blocking G-CSF but not IL-1R signaling in vivo rescues this neutrophilia, suggesting that a G-CSF–dependent, IL-1β–independent pathway plays a role in promoting neutrophil production in mice with defective clearance of apoptotic cells.

scholarly journals Caspase-9 mediates the apoptotic death of megakaryocytes and platelets, but is dispensable for their generation and function

Blood ◽  
2012 ◽  
Vol 119 (18) ◽  
pp. 4283-4290 ◽  
Author(s):  
Michael J. White ◽  
Simone M. Schoenwaelder ◽  
Emma C. Josefsson ◽  
Kate E. Jarman ◽  
Katya J. Henley ◽  
...  
Keyword(s):  
Steady State ◽  
Caspase Activation ◽  
Caspase 9 ◽  
Platelet Production ◽  
Effector Caspase ◽  
Functional Regulation ◽  
Caspase Cascade ◽  
And Function

Abstract Apoptotic caspases, including caspase-9, are thought to facilitate platelet shedding by megakaryocytes. They are known to be activated during platelet apoptosis, and have also been implicated in platelet hemostatic responses. However, the precise requirement for, and the regulation of, apoptotic caspases have never been defined in either megakaryocytes or platelets. To establish the role of caspases in platelet production and function, we generated mice lacking caspase-9 in their hematopoietic system. We demonstrate that both megakaryocytes and platelets possess a functional apoptotic caspase cascade downstream of Bcl-2 family-mediated mitochondrial damage. Caspase-9 is the initiator caspase, and its loss blocks effector caspase activation. Surprisingly, steady-state thrombopoiesis is unperturbed in the absence of caspase-9, indicating that the apoptotic caspase cascade is not required for platelet production. In platelets, loss of caspase-9 confers resistance to the BH3 mimetic ABT-737, blocking phosphatidylserine (PS) exposure and delaying ABT-737–induced thrombocytopenia in vivo. Despite this, steady-state platelet lifespan is normal. Casp9−/− platelets are fully capable of physiologic hemostatic responses and functional regulation of adhesive integrins in response to agonist. These studies demonstrate that the apoptotic caspase cascade is required for the efficient death of megakaryocytes and platelets, but is dispensable for their generation and function.

A Novel Role of Histone Deacetylase 11 (HDAC11) in Regulation of Myeloid-Derived Suppressor Cell (MDSC) Expansion

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2439-2439
Author(s):  
Eva Sahakian ◽  
John Powers ◽  
Jennifer Rock-Klotz ◽  
Marsilio Adriani ◽  
Karrune V. Woan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Steady State ◽  
Transgenic Mice ◽  
Myeloid Cells ◽  
Negative Regulator ◽  
Cell Phenotype ◽  
Variable Expression ◽  
Tumor Bearing

Abstract Abstract 2439 HDAC11 is the newest member of the HDAC family. The physiological role of this HDAC was largely unknown until the discovery by our group that HDAC11 regulates IL-10 gene expression in myeloid cells in-vitro1. To better elucidate the role of HDAC11 in these cells, we have utilized an HDAC11 promoter-driven eGFP reporter transgenic mice (TgHDAC11-eGFP) which allow us to “visualize” dynamic changes in HDAC11 gene expression /transcriptional activity in immune cells in vivo. Immature myeloid cells (IMCs) differentiate into dendritic cells, macrophages, and neutrophils and are also considered to be precursors of MDSCs in tumor-bearing hosts. Here, we show for the first time that HDAC11 plays an important role in this process. First, IMCs from the bone marrow and spleen of TgHDAC11-eGFP mice display high expression of eGFP indicative of HDAC11 transcriptional activation in these cells in the steady state. Subcutaneous injection of PANCO2 tumor cells into these mice resulted in expansion of MDSCs (identified by the expression of CD11b+/GR1+ [Ly6G and Ly6C] with variable expression of CD49d and CD115) in their lymphoid organs which was similar in magnitude to the expansion observed in tumor-bearing wild type (WT) mice. Of note, flow cytometric analysis revealed that expression of eGFP was significantly decreased in the myeloid compartment of tumor bearing TgHDAC11-eGFP mice, suggesting that the transition of IMC into MDSCs might require a decrease in HDAC11 expression. Reminiscent of our findings in the eGFP mice, studies in non-transgenic mice also demonstrated that tumor derived CD11b+ Ly6G+ MDSCs display less HDAC11 mRNA expression. Additional support for the regulatory role of HDAC11 in MDSC expansion/function has been recently provided by our studies in HDAC11KO mice, demonstrating the acquisition of a suppressive cell phenotype, by myeloid cells identical to MDSCs, in the steady state and in the absence of tumor challenge. Taken together, HDAC11 might function as a negative regulator of MDSC expansion/function in vivo. A better understanding of this previously unknown role of HDAC11 in MDSC biology might lead to targeted epigenetic therapies to influence the suppressive abilities of these cells and augment the efficacy of immunotherapeutic approaches against hematologic malignancies. 1. Villagra A, et al. Nat Immunol. 2009 Jan;10(1):92-100 Disclosures: No relevant conflicts of interest to declare.

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