Isolation and evaluation of oil-producing microalgae from subtropical coastal and brackish waters

Microalgae have been widely reported as a promising source of biofuels, mainly based on their high areal productivity of biomass and lipids as triacylglycerides and the possibility for cultivation on non-arable land. The isolation and selection of suitable strains that are robust and display high growth and lipid accumulation rates is an important prerequisite for their successful cultivation as a bioenergy source, a process that can be compared to the initial selection and domestication of agricultural crops. We developed standard protocols for the isolation and cultivation for a range of marine and brackish microalgae. By comparing growth rates and lipid productivity, we assessed the potential of subtropical coastal and brackish microalgae for the production of biodiesel and other oil-based bioproducts. This study identified Nannochloropsis sp., Dunaniella salina and new isolates of Chlorella sp. and Tetraselmis sp. as suitable candidates for a multiple-product algae crop. We conclude that subtropical coastal microalgae display a variety of fatty acid profiles that offer a wide scope for several oil-based bioproducts, including biodiesel and omega-3 fatty acids. A biorefinery approach for microalgae would make economical production more feasible but challenges remain for efficient harvesting and extraction processes for some species.     

Fatty acid analysis of four Azospirillum species reveals three groups

Cellular fatty acid composition of 14 strains from the four species of Azospirillum was determined by gas chromatographic analysis. All strains of Azospirillum lipoferum and Azospirillum brasilense were similar in fatty acid data, thus not revealing an expected distinction between the two long established species. Strains of both Azospirillum halopraeferens and Azospirillum amazonense, however, differed significantly from this first group of strains.     

Zur osmotischen Beeinflussung der Photosynthese von Cyanophora paradoxa Korsch. durch Saccharose

Zusammenfassung Die Geschwindigkeit der photosynthetischen Sauerstoffentwicklung des sich recht langsam vermehrenden Cyanoms Cyanophora paradoxa ist nur geringfügig niedriger als diejenige anderer Algen (in bezug auf die Chlorophyllkonzentration). Merkwürdigerweise stellt man eine starke Abhängigkeit photosynthetischer Reaktionen (O₂-Entwicklung, CO₂ Fixierung und Hill-Reaktion mit 2,6-Dichlorphenolindophenol) von der im Medium vorgegebenen Konzentration eines Osmotikums fest. Unter bestimmten Voraussetzungen können steigende Saccharosekonzentrationen (bis ca. 0,1 M) die assimilatorische Sauerstoffproduktion zunächst beschleunigen, höhere Saccharose-Konzentrationen (über 0,1 M) hemmen dagegen. Der Hemmeffekt ist unspezifisch und kann auch in Abhängigkeit von Sorbit und Natriumchlorid beobachtet werden. Die bisherigen Versuche sprechen dafür, daß der Hemmeffekt bis zu einer Konzentration von ca. 0,1 M Saccharose während kurzer Einwirkungszeit reversibel ist, bei höheren Konzentrationen jedoch schon irreversible Zellschädigungen anzeigt.

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Sucrose as an effector of photosynthesis in Cyanophora paradoxa korsch

Cyanophora paradoxa, a fresh-water alga, was found to evolve oxygen photosynthetically with activities similar to other plants (50–300 mol O₂/mg chlorophyll·h). In spite of this the doubling time was 10–30 days. The photosynthetic activity turned out to react very sensitively to external osmotic concentrations. In lower concentrations as conventionally used for chloroplast preparations, sucrose—partially irreversibly—inhibited both photosynthetic O₂ evolution and Hill reaction with 2,6-Dichlorophenolindophenol progressively between 0.1 and 0.5 M. Sorbitol and sodium chloride had similar effects. In a medium of low osmolarity (0.025–0.1 M sucrose) the photosynthetic activity was increased. These results were interpreted as consequence of osmotic interactions between the cell and its environment. When the cells are unable to correct the external osmotic pressure, an irreversible degradation of intracellular membranes is initiated, which finally leads to a total decomposition of the eukaryotic cell.

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Abkurzungen EDTA Athylendiamintetraessigsäure - DCPIP 2,6-Dichlorphenolindophenol     

Improving ability to identify malaria and correctly use chloroquine in children at household level in Nakonde District, Northern Province of Zambia

BACKGROUND: This study investigated causes of malaria and how cases were managed at household level, in order to improve the ability to identify malaria and ensure correct use of chloroquine. It was conducted in Nakonde District, Northern Province of Zambia, between 2000 and 2001. Nakonde district is in a hyperendemic malaria province, where Plasmodium falciparum is predominant. The district has a total population of 153, 548 people, the majority of whom are peasant farmers. The main aim of the post intervention survey was to establish the proportion of caretakers of children five years and below, who were able to identify simple and severe malaria and treat it correctly using chloroquine in the home. METHODS: A baseline survey was conducted in five wards divided into intervention and control.Intervention and control wards were compared. Village health motivators and vendors were identified and trained in three intervention wards, as a channel through which information on correct chloroquine dose could be transmitted. A total of 575 carers, who were 15 years old and above and had a child who had suffered from malaria 14 days before the survey commenced, were interviewed. The two control wards received no intervention. 345 caretakers were from the intervention wards, while 230 came from the control wards. Identification of malaria and correct use of anti-malarial drugs was assessed in terms of household diagnosis of malaria in children under five years, type and dose of anti-malarial drugs used, self medication and the source of these anti-malarials. RESULTS: The majority of respondents in the study were females (81%). Chloroquine was the most frequently used anti-malarial (48.5%) in both the intervention and control wards. There was no difference between the intervention and control wards at pre-intervention (P = 0.266 and P = 0.956), in the way mothers and other caretakers identified simple and severe malaria. At baseline, knowledge on correct chloroquine dosage in the under five children was comparable between intervention and control wards. Post-intervention revealed that mothers and other caretakers were 32% and 51%, respectively, more likely to identify simple and severe malaria. There was a 60% increase on correct chloroquine dosage in all age groups among carers living in post-intervention wards. CONCLUSION: Compliance with standard therapeutic doses and correct identification of malaria was poorest in control wards, where no motivators and vendors were trained.     

Cartilage ultrastructure after high pressure freezing, freeze substitution, and low temperature embedding. I. Chondrocyte ultrastructure--implications for the theories of mineralization and vascular invasion

Electron microscopic examination of epiphyseal cartilage tissue processed by high pressure freezing, freeze substitution, and low temperature embedding revealed a substantial improvement in the preservation quality of intracellular organelles by comparison with the results obtained under conventional chemical fixation conditions. Furthermore, all cells throughout the epiphyseal plate, including the terminal chondrocyte adjacent to the region of vascular invasion, were found to be structurally integral. A zone of degenerating cells consistently observed in cartilage tissue processed under conventional chemical fixation conditions was not apparent. Hence, it would appear that cell destruction in this region occurs during chemical processing and is not a feature of cartilage tissue in the native state. Since these cells are situated in a region where tissue calcification is taking place, the implication is that the onset and progression of cartilage calcification are, at least partially, controlled by the chondrocytes themselves. The observation that the terminal cell adjacent to the zone of vascular invasion is viable has important implications in relation to the theory of vascular invasion. This may now require reconceptualization to accommodate the possibility that active cell destruction may be a precondition for vascular invasion.     

Bioimpedance Identifies Body Fluid Loss after Exercise in the Heat: A Pilot Study with Body Cooling

Purpose

Assessment of post-exercise changes in hydration with bioimpedance (BI) is complicated by physiological adaptations that affect resistance (R) and reactance (Xc) values. This study investigated exercise-induced changes in R and Xc, independently and in bioelectrical impedance vector analysis, when factors such as increased skin temperature and blood flow and surface electrolyte accumulation are eliminated with a cold shower.

Methods

Healthy males (n = 14, 24.1±1.7 yr; height (H): 182.4±5.6 cm, body mass: 72.3±6.3 kg) exercised for 1 hr at a self-rated intensity (15 BORG) in an environmental chamber (33°C and 50% relative humidity), then had a cold shower (15 min). Before the run BI, body mass, hematocrit and Posm were measured. After the shower body mass was measured; BI measurements were performed continuously every 20 minutes until R reached a stable level, then hematocrit and Posm were measured again.

Results

Compared to pre-trial measurements body mass decreased after the run and Posm, Hct, R/H and Xc/H increased (p<0.05) with a corresponding lengthening of the impedance vector along the major axis of the tolerance ellipse (p<0.001). Changes in Posm were negatively related to changes in body mass (r = −0.564, p = 0.036) and changes in Xc/H (r = −0.577, p = 0.041).

Conclusions

Present findings showed that after a bout of exercise-induced dehydration followed by cold shower the impedance vector lengthened that indicates fluid loss. Additionally, BI values might be useful to evaluate fluid shifts between compartments as lower intracellular fluid loss (changed Xc/R) indicated greater Posm increase.     

Carboxy-Terminal Modulator Protein (CTMP) is a mitochondrial protein that sensitizes cells to apoptosis

The Carboxy-Terminal Modulator Protein (CTMP) protein was identified as a PKB inhibitor that binds to its hydrophobic motif. Here, we report mitochondrial localization of endogenous and exogenous CTMP. CTMP exhibits a dual sub-mitochondrial localization as a membrane-bound pool and a free pool of mature CTMP in the inter-membrane space. CTMP is released from the mitochondria into the cytosol early upon apoptosis. CTMP overexpression is associated with an increase in mitochondrial membrane depolarization and caspase-3 and polyADP-ribose polymerase (PARP) cleavage. In contrast, CTMP knock-down results in a marked reduction in the loss of mitochondrial membrane potential as well as a decrease in caspase-3 and PARP activation. Mutant CTMP retained in the mitochondria loses its capacity to sensitize cells to apoptosis. Thus, proper maturation of CTMP is essential for its pro-apoptotic function. Finally, we demonstrate that CTMP delays PKB phosphorylation following cell death induction, suggesting that CTMP regulates apoptosis via inhibition of PKB.     

Grey matter damage in multiple sclerosis

Over the past decade, immunohistochemical studies have provided compelling evidence that gray matter (GM) pathology in multiple sclerosis (MS) is extensive. Until recently, this GM pathology was difficult to visualize using standard magnetic resonance imaging (MRI) techniques. However, with newly developed MRI sequences, it has become clear that GM damage is present from the earliest stages of the disease and accrues with disease progression. GM pathology is clinically relevant, as GM lesions and/or GM atrophy were shown to be associated with MS motor deficits and cognitive impairment. Recent autopsy studies demonstrated significant GM demyelination and microglia activation. However, extensive immune cell influx, complement activation and blood-brain barrier leakage, like in WM pathology, are far less prominent in the GM. Hence, so far, the cause of GM damage in MS remains unknown, although several plausible underlying pathogenic mechanisms have been proposed. This paper provides an overview of GM damage in MS with a focus on its topology and histopathology.