Surveys of the California Current System in 1993 revealed high concentrations of photosynthetic pigment biomass at -200-m depth, well below the euphotic zone. The deep fluorescence feature contained an estimated 2.2 X 10J metric tons of carbon and contained -2.5 times the amount of chloroph,yll observed in surface waters directly above it. Deep phytoplankton assemblages may be a signature of water mass subduction, suggesting the possibility of using phytoplankton as water mass tracers. These field observations led to a laboratory study of the fluorescence characteristics of autotrophic cells as possible indices of acclimation to extended periods of darkness. In vivo multiexcitation Chl a fluorescence of the diatom Thalassiosira weissflogii was mlsnitored for 2 months of total darkness. Numbers of living and dead cells were determined using the vital stain flucarescein diacetate (FDA). By the end of the dark incubation period, in vivo Chl a fluorescence and fluorescence per cell had leveled off to -45% and 65% of initial values, respectively. The contribution of accessory pigments to Chl a fluorescence, expressed as multiexcitation fluorescence ratios, was higher in the dark than prior to transfer to darkness but showed no significant changes during 2 months of darkness. The FDA assay indicated that -85% of the cells were alive for at least the first 3 weeks during the first dark experiment and for the entire 2 months of 1 second dark incubation. Cell numbers decreased to 65% of initial values and then grew exponentially upon reexplsure to a light: dark photoperiod. Our results for T. weissjlogii suggest that extended light limitation of photosynthesis does not preclude the survival of subducted phytoplankton assemblages and the consequent accumulation of Chl a at depths below the euphotic zone. If these results extend to natural assemblages, it is not possible to estimate advective time scales based on a maximum persistence time of pigment fluorescence below the euphotic zone. Nevertheless, the deep phytoplankton assemblage we observed provides evidence for water mass subduction and suggests that large, intermittent pulses of phytoplankton carbon are a part of cross-shelf exchange and vertical flux from surface waters to depth in this region.
Low-grade inflammation is often an underlying cause of several chronic diseases such as asthma, obesity, cardiovascular disease, and type 2 diabetes mellitus (T2DM). Defining the mediators of such chronic low-grade inflammation often appears dependent on which disease is being investigated. However, downstream systemic inflammatory cytokine responses in these diseases often overlap, noting there is no doubt more than one factor at play to heighten the inflammatory response. Furthermore, it is increasingly believed that diet and an altered gut microbiota may play an important role in the pathology of such diverse diseases. More specifically, the inflammatory mediator endotoxin, which is a complex lipopolysaccharide (LPS) derived from the outer membrane cell wall of Gram-negative bacteria and is abundant within the gut microbiota, and may play a direct role alongside inhaled allergens in eliciting an inflammatory response in asthma. Endotoxin has immunogenic effects and is sufficiently microscopic to traverse the gut mucosa and enter the systemic circulation to act as a mediator of chronic low-grade inflammation in disease. Whilst the role of endotoxin has been considered in conditions of obesity, cardiovascular disease and T2DM, endotoxin as an inflammatory trigger in asthma is less well understood. This review has sought to examine the current evidence for the role of endotoxin in asthma, and whether the gut microbiota could be a dietary target to improve disease management. This may expand our understanding of endotoxin as a mediator of further low-grade inflammatory diseases, and how endotoxin may represent yet another insult to add to injury.
Context Dysfunctional endoplasmic reticulum (ER) and mitochondria are known to contribute to the pathology of metabolic disease. This damage may occur, in part, as a consequence of ER-mitochondria cross-talk in conditions of nutrient excess such as obesity. To date, insight into this dynamic relationship has not been characterized in adipose tissue. Therefore, this study investigated whether ER stress contributes to the development of mitochondrial inefficiency in human adipocytes from lean and obese participants. Methods Human differentiated adipocytes from Chub-S7 cell line and primary abdominal subcutaneous adipocytes from lean and obese participants were treated with tunicamycin to induce ER stress. Key parameters of mitochondrial function were assessed, including mitochondrial respiration, membrane potential (MMP), and dynamics. Results ER stress led to increased respiratory capacity in a model adipocyte system (Chub-S7 adipocytes) in a concentration and time dependent manner (24 h: 23%↑; 48 h: 68%↑, P < 0.001; 72 h: 136%↑, P < 0.001). This corresponded with mitochondrial inefficiency and diminished MMP, highlighting the formation of dysfunctional mitochondria. Morphological analysis revealed reorganization of mitochondrial network, specifically mitochondrial fragmentation. Furthermore, p-DRP1, a key protein in fission, significantly increased (P < 0.001). Additionally, adipocytes from obese subjects displayed lower basal respiration (49%↓, P < 0.01) and were unresponsive to tunicamycin in contrast to their lean counterparts, demonstrating inefficient mitochondrial oxidative capacity. Conclusion These human data suggest that adipocyte mitochondrial inefficiency is driven by ER stress and exacerbated in obesity. Nutrient excess–induced ER stress leads to mitochondrial dysfunction that may therefore shift lipid deposition ectopically and thus have further implications on the development of related metabolic disorders.
Several species and genera of very small diatoms have been isolated from Gulf of Mexico waters at Galveston. A quantitative and qualitative study of their distribution has not yet been made. The organisms were isolated in unialgal cultures, and very rapid growth rates were observed. Environmental and experimental implications are pointed out. A new species, Chaetoceros galvestonensis, 1.5 by 3.0 microns in broad view, is described and figured.
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