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A time-dependent model of Margalefidinium polykrikoides, a mixotrophic dinoflagellate, cell growth was implemented to assess controls on blooms in the Lafayette River, a shallow, tidal sub-tributary of the lower Chesapeake Bay. Simulated cell growth included autotrophic and heterotrophic contributions. Autotrophic cell growth with no nutrient limitation resulted in a bloom but produced chlorophyll concentrations that were 45% less than observed bloom concentrations (~80 mg Chl m -3 vs. 145 mg Chl m -3 ) and a bloom progression that did not match observations. Excystment (cyst germination) was important for bloom initiation, but did not influence the development of algal biomass or bloom duration. Encystment (cyst formation) resulted in small losses of biomass throughout the bloom but similarly, did not influence M. polykrikoides cell density or the duration of blooms. In contrast, the degree of heterotrophy significantly impacted cell densities achieved and bloom duration. When heterotrophy contributed a constant 30% to cell growth, and dissolved inorganic nitrogen was not limiting, simulated chlorophyll concentrations were within those observed during blooms (maximum ~140 mg Chl m -3 ). However, nitrogen limitation quenched the maximum chlorophyll concentration by a factor of three. Specifying heterotrophy as an increasing function of nutrient limitation, allowing it to contribute up to 50% and 70% of total growth, resulted in simulated maximum chlorophyll concentrations of 90 mg Chl m -3 and 180 mg Chl m -3 , respectively. This suggested that blooms of M. polykrikoides in the Lafayette River are fortified and maintained by substantial heterotrophic nutritional inputs. The timing and progression of the simulated bloom was controlled by the temperature range, 23 °C to 28 °C, that supports M. polykrikoides growth. Temperature increases of 0.5 °C and 1.0 °C, consistent with current warming trends in the lower Chesapeake Bay due to climate change, shifted the timing of bloom initiation to be earlier and extended the duration of blooms; maximum bloom magnitude was reduced by 50% and 65%, respectively. Warming by 5 °C suppressed the summer bloom. The simulations suggested that the timing of M. polykrikoides blooms in the Lafayette River is controlled by temperature and the bloom magnitude is determined by trade-offs between the severity of nutrient limitation and the relative contribution of mixotrophy to cell growth., (Copyright © 2021. Published by Elsevier B.V.)

Aquaporin-4, present in ependymal cells, in glia limiting and abundantly in pericapillary astrocyte foot processes, and aquaporin-1, expressed in choroid plexus epithelial cells, play an important role in cerebrospinal fluid production and may be involved in the pathophysiology of age-dependent hydrocephalus. The finding that brain aquaporins expression is regulated by low oxygen tension led us to investigate how hypoxia and elevated levels of cerebral aquaporins may result in an increase in cerebrospinal fluid production that could be associated with a hydrocephalic condition. Here we have explored, in young and aged mice exposed to hypoxia, whether aquaporin-4 and aquaporin-1 participate in the development of age-related hydrocephalus. Choroid plexus, striatum, cortex and ependymal tissue were analyzed separately both for mRNA and protein levels of aquaporins. Furthermore, parameters such as total ventricular volume, intraventricular pressure, cerebrospinal fluid outflow rate, ventricular compliance and cognitive function were studied in wild type, aquaporin-1 and aquaporin-4 knock-out animals subjected to hypoxia or normoxia. Our data demonstrate that hypoxia is involved in the development of age-related hydrocephalus by a process that depends on aquaporin-4 channels as a main route for cerebrospinal fluid movement. Significant increases in aquaporin-4 expression that occur over the course of animal aging, together with a reduced cerebrospinal fluid outflow rate and ventricular compliance, contribute to produce more severe hydrocephalus related to hypoxic events in aged mice, with a notable impairment in cognitive function. These results indicate that physiological events and/or pathological conditions presenting with cerebral hypoxia/ischemia contribute to the development of chronic adult hydrocephalus., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Intrastriatal transplantation of dopaminergic carotid body (CB) cells ameliorates parkinsonism in animal models and, with less efficacy, in Parkinson's disease patients. CB-based cell therapy was initially proposed because of its high dopamine content. However, later studies suggested that its beneficial effect might be due to a trophic action exerted on nigrostriatal neurons. Compatible with this concept are the high levels of neurotrophic factors encountered in CB cells. To test experimentally this idea, unilateral striatal transplants were performed with a sham graft in the contralateral striatum, as a robust internal control. Thereafter, the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6, -tetrahydropyridine was injected during 3 months. CB grafts protected from degeneration ipsilateral nigral dopaminergic neurons projecting to the transplant in a dose-dependent manner regarding size and glial cell line-derived neurotrophic factor expression. Grafts performed at different times after the onset of the neurotoxic treatment demonstrated with histological and behavioral methods protection and repair of the nigrostriatal pathway by CB transplants. This study provides a mechanistic explanation for the action of CB transplants on parkinsonian models. It should also help to improve cell therapy approaches to Parkinson's disease., (Copyright © 2013 Elsevier Inc. All rights reserved.)

The Kid and Kis proteins are the killer component and the antagonist belonging to parD, a killer stability system of plasmid R1. The Kid and Kis proteins have been purified, the second one as a C-LYT-Kis fusion that conserves the antagonistic activity of the Kis protein, but not its auto-regulatory potential. Kid inhibits in vitro replication of CoEl to a basal level without altering the superhelicity of the template but it does not substantially affect in vitro replication of P4, a DnaA, DnaB, DnaC and DnaG-independent replicon. Kid inhibits lytic induction of a lambda, prophage, but this inhibition can be neutralized by excess DnaB. In addition, a multicopy dnaB recombinant, but not a multicopy dnaG recombinant, prevents the toxicity associated with this protein. Inhibition of ColE1 replication by Kid in vitro is prevented by the C-LYT-Kis protein. Functional analysis indicates that the antagonistic activity of Kis is independent of its activity as a co-regulator of the parD promoter. It is also shown that C-LYT-Kis and Kid interact, forming a tight complex. These results strongly suggest that the toxicity of the kid protein is due to inhibition of DnaB-dependent DNA replication, and that direct protein-protein interactions are involved in the neutralization of the activity of the killer protein by the antagonist.

Transcription of the repA gene of the Pseudomonas plasmid pPS10 is initiated from a sigma 70 type promoter located 81 bp upstream from the repA gene, extends through the repA gene and the adjacent open reading frame, and ends 1114 nucleotides downstream. The repA promoter is repressed by interactions of the RepA protein with a region of 44 bp that extends from the -10 box of the promoter to the dnaA box of the origin of replication. The core of the repA operator region is formed by two in-phase invertedly repeated sequences of 8 bp, S1 and S2, that flank the -35 box of the promoter, and that share homology with the internal sequences of the iterons present in the origin of replication. RepA enters at the operator region first by protein-DNA interactions and subsequently by protein-protein interactions. These sequential interactions lead to the formation of high, medium and low-mobility electrophoretic complexes. Formation of the high-order complexes seems to be important for an efficient repression of the promoter. Interactions of RepA with the repA promoter region (repPO) occur more efficiently than with the origin of replication.