Effects of some salts and sodicity on the growth of a Rhizobium leguminosarum bv. viceae strain isolated from a salt-affected soil.

The effects of sodium (Na+), calcium (Ca2+), magnesium (Mg2+), and boron (B) concentrations and sodicity, as measured by the sodium adsorption ratio (SAR), on the growth of a Rhizobium leguminosarum bv. viceae strain isolated from a salt-affected soil were studied. The rate of growth was measured in a yeast extract-mannitol broth, amended with salts having electrical conductivity (EC) of 4, 8, and 16 dS x m(-1). Each salinity level was prepared to achieve SAR values of 10, 20, and 30 with or without graded B concentrations of 0.5, 1, 3, and 5 mg x L(-1). We found that salinity levels equal to or more than 8 dS x m(-1) had negative effects on Rhizobium growth during the first days of incubation, but the effects became less pronounced after 1 week. Na+ concentrations of more than 1.1 g x L(-1) retarded growth, especially at high SAR values (i.e., at low Ca2+ concentrations). The retardation of growth increased with increases in EC up to 16 dS x m(-1), at all sodicity levels. Mg2+ added together with Na+ or with Ca2+ + Na+ affected growth more negatively than Ca2+ + Na+ alone. The effect of Mg2+ became more pronounced with increased salinities and sodicities. It was concluded that EC of more than 4 dS x m(-1) retarded growth of Rhizobium, but only at high sodicity levels. The relative specific ion effect on growth was in the order Na+ < Ca2+ < Mg2+. The harmful effect of Mg2+ on this strain was accentuated by adding Ca2+ to the cultural medium. When SAR increased from 10 to 30, Na+ had no clear effect on growth, irrespective of the accompanied cations, i.e, Ca2+, Mg2+, or Ca2+ + Mg2+. Growth was reduced by B concentrations as low as 0.5 mg x L(-1), and the B effect was enhanced by increased salinity.     

Neurotrophic factors in Alzheimer's disease: role of axonal transport

Neurotrophic factors (NTF) are small, versatile proteins that maintain survival and function to specific neuronal populations. In general, the axonal transport of NTF is important as not all of them are synthesized at the site of its action. Nerve growth factor (NGF), for instance, is produced in the neocortex and the hippocampus and then retrogradely transported to the cholinergic neurons of the basal forebrain. Neurodegenerative dementias like Alzheimer's disease (AD) are linked to deficits in axonal transport. Furthermore, they are also associated with imbalanced distribution and dysregulation of NTF. In particular, brain-derived neurotrophic factor (BDNF) plays a crucial role in cognition, learning and memory formation by modulating synaptic plasticity and is, therefore, a critical molecule in dementia and neurodegenerative diseases. Here, we review the changes of NTF expression and distribution (NGF, BDNF, neurotrophin-3, neurotrophin-4/5 and fibroblast growth factor-2) and their receptors [tropomyosin-related kinase (Trk)A, TrkB, TrkC and p75^NTR] in AD and AD models. In addition, we focus on the interaction with neuropathological hallmarks Tau/neurofibrillary tangle and amyloid-β (Abeta)/amyloid plaque pathology and their influence on axonal transport processes in order to unify AD-specific cholinergic degeneration and Tau and Abeta misfolding through NTF pathophysiology.     

Carboxymethyl cellulose and Pluronic F68 protect the dinoflagellate Protoceratium reticulatum against shear-associated damage

The red-tide dinoflagellate Protoceratium reticulatum is shown to be protected against turbulence-associated damage by the use of the additives Pluronic F68 (PF68) and carboxymethyl cellulose (CMC) in the culture medium. Relative to agitated controls, these additives had a dose-dependent protective effect at concentrations of up to 0.4 and 0.5 g L⁻¹ for CMC and F68, respectively. In static cultures, these additives inhibited growth directly or indirectly at a concentration of >0.5 g L⁻¹. Compared to CMC, PF68 was a better protectant overall. Cell-specific production of yessotoxins was enhanced under elevated shear stress regimens so long as the turbulence intensity was insufficient to damage the cells outright. Shear-induced production of reactive oxygen species and direct effects of turbulence on the cell cycle contributed to the observed shear effects.     

NADPH oxidases in Parkinson’s disease: a systematic review

Parkinson’s disease (PD) is a progressive movement neurodegenerative disease associated with a loss of dopaminergic neurons in the substantia nigra of the brain. Oxidative stress, a condition that occurs due to imbalance in oxidant and antioxidant status, is thought to play an important role in dopaminergic neurotoxicity. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases are multi-subunit enzymatic complexes that generate reactive oxygen species as their primary function. Increased immunoreactivities for the NADPH oxidases catalytic subunits Nox1, Nox2 and Nox4 have been reported in the brain of PD patients. Furthermore, knockout or genetic inactivation of NADPH oxidases exert a neuroprotective effect and reduce detrimental aspects of pathology in experimental models of the disease. However, the connections between NADPH oxidases and the biological processes believed to contribute to neuronal death are not well known. This review provides a comprehensive summary of our current understanding about expression and physiological function of NADPH oxidases in neurons, microglia and astrocytes and their pathophysiological roles in PD. It summarizes the findings supporting the role of both microglial and neuronal NADPH oxidases in cellular disturbances associated with PD such as neuroinflammation, alpha-synuclein accumulation, mitochondrial and synaptic dysfunction or disruption of the autophagy-lysosome system. Furthermore, this review highlights different steps that are essential for NADPH oxidases enzymatic activity and pinpoints major obstacles to overcome for the development of effective NADPH oxidases inhibitors for PD.     

Eicosapentaenoic and arachidonic acids purification from the red microalga Porphyridium cruentum

The polyunsaturated fatty acids (PUFA) eicosapentaenoic and arachidonic acids (EPA and AA), which have several pharmaceutical properties, have been purified from the red microalga Porphyridium cruentum. The process consists of only four main steps: (i) simultaneous extraction and saponification of the microalgal biomass; (ii) urea inclusion method (iii) PUFA esterification (iv) argentated silica gel column chromatography of the urea concentrate. Total AA and EPA recoveries reached 39.5% and 50.8% respectively for a purity 97% for both fatty acids. Therefore, recovery of highly pure PUFA could be improved in organisms that are rich in two or more fatty acids of interest. The results of several procedures for AA and EPA recovery from several authors by using this microalga were compared.     

New culture approaches for yessotoxin production from the dinoflagellate Protoceratium reticulatum

Fed-batch and perfusion cultures were carried out in a traditional glass 2-L bioreactor with the toxic dinoflagellate Protoceratium reticulatum. The maximum cell concentration obtained was 2.3 x 105 cell.mL-1, which is almost 1 order of magnitude higher than the maximum previously referenced for this species. L1 medium was shown to be clearly deficient in nitrate and phosphate for this strain, and addition of highly concentrated aliquots of these nutrients allowed higher cell concentrations to be obtained. This species consumed high amounts of nitrate and phosphate, 2.1 x 10-3 and 2.3 x 10-4 micromol.h-1.cell-1, respectively. However, this consumption produced a very low number of cells compared to other classes of microalgae, indicating that this species is, like other dinoflagellates, a poor competitor in terms of utilization of inorganic nutrients. Higher production of toxins and pigments was strongly associated with cell number in the culture, with maximum values of 700 ng.mL-1 and 1321 microg.mL-1, respectively. Most yessotoxins remained within the cells and not in the cell-free culture medium, and their production was not related to either the age of the culture or the cell growth phase.     

A bioreaction–diffusion model for growth of marine sponge explants in bioreactors

Marine sponges are sources of high-value bioactives. Engineering aspects of in vitro culture of sponges from cuttings (explants) are poorly understood. This work develops a diffusion-controlled growth model for sponge explants. The model assumes that the explant growth is controlled by diffusive transport of at least some nutrients from the surrounding medium into the explant that generally has a poorly developed aquiferous system for internal irrigation during early stages of growth. Growth is assumed to obey Monod-type kinetics. The model is shown to satisfactorily explain the measured growth behavior of the marine sponge Crambe crambe in two different growth media. In addition, the model is generally consistent with published data for growth of explants of the sponges Disidea avara and Hemimycale columella. The model predicted that nutrient concentration profiles for nutrients, such as dissolved oxygen within the explant, are consistent with data published by independent researchers. In view of the proposed model’s ability to explain available data for growth of several species of sponge explants, diffusive transport does play a controlling role in explant growth at least until a fully developed aquiferous system has become established. According to the model and experimental observations, the instantaneous growth rate depends on the size of the explant and all those factors that influence the diffusion of critical nutrients within the explant. Growth follows a hyperbolic profile that is consistent with the Monod kinetics.     

Induction of CD40 expression and enhancement of monoclonal antibody production on murine B cell hybridomas by cross-linking of IgG receptors

The 55-6 murine B cell hybridoma line not constitutively expressing CD40 was treated with increasing amounts of intact anti-mouse surface immunoglobulin G antibody (anti-mIgG) either not preincubated or preincubated for 48 h with lipopolysaccharide (LPS). In vitro, cross-linking of surface immunoglobulin G (sIgG) with the whole molecule of anti-IgG antibodies induced the expression of CD69, CD40, and CD19 surface antigens on 55-6 cells. The effect of sIgG ligation was dose-dependent, and preincubation with LPS enhanced their responsiveness to anti-mIgG stimulation. The expression of these surface molecules reached the maximum value during the first part of the cell cycle, corresponding to the position of the G1 peak of the DNA distribution. Stimulation of cells with anti-mIgG did not induce changes either in the number of viable cells or in the fraction of cells undergoing proliferation (mitosis). However, preincubation of 55-6 cells with LPS for 48 h before stimulation with anti-mIgG increased both the maximum specific growth rate (micromax) and the percentage of cells in the G2/M phase, in comparison with non-preincubated cells. Moreover, on cells preincubated with LPS prior to anti-mIgG treatment, specific IgG2a production rate was enhanced significantly compared to that obtained in control cultures. The correlation between the antibody production rate and the amount of IgG that is detectable on the cell surface was analyzed by flow cytometry. A good correlation between secreted and surface IgG was observed, and the results of cell cycle analyses demonstrated that the 55-6 hybridoma cell line has a substantially higher sIgG content in G1 phase.