Climate change and freshwater biodiversity: detected patterns, future trends and adaptations in northern regions

Current rates of climate change are unprecedented, and biological responses to these changes have also been rapid at the levels of ecosystems, communities, and species. Most research on climate change effects on biodiversity has concentrated on the terrestrial realm, and considerable changes in terrestrial biodiversity and species’ distributions have already been detected in response to climate change. The studies that have considered organisms in the freshwater realm have also shown that freshwater biodiversity is highly vulnerable to climate change, with extinction rates and extirpations of freshwater species matching or exceeding those suggested for better‐known terrestrial taxa. There is some evidence that freshwater species have exhibited range shifts in response to climate change in the last millennia, centuries, and decades. However, the effects are typically species‐specific, with cold‐water organisms being generally negatively affected and warm‐water organisms positively affected. However, detected range shifts are based on findings from a relatively low number of taxonomic groups, samples from few freshwater ecosystems, and few regions. The lack of a wider knowledge hinders predictions of the responses of much of freshwater biodiversity to climate change and other major anthropogenic stressors. Due to the lack of detailed distributional information for most freshwater taxonomic groups and the absence of distribution‐climate models, future studies should aim at furthering our knowledge about these aspects of the ecology of freshwater organisms. Such information is not only important with regard to the basic ecological issue of predicting the responses of freshwater species to climate variables, but also when assessing the applied issue of the capacity of protected areas to accommodate future changes in the distributions of freshwater species. This is a huge challenge, because most current protected areas have not been delineated based on the requirements of freshwater organisms. Thus, the requirements of freshwater organisms should be taken into account in the future delineation of protected areas and in the estimation of the degree to which protected areas accommodate freshwater biodiversity in the changing climate and associated environmental changes.     

Identification of novel splice variants of ARNT and ARNT2 in the rat

Most of the biochemical and toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are mediated by the bHLH/PAS protein AH receptor (AHR). For regulation of gene activities, AHR dimerizes with another member of the bHLH/PAS protein family, AHR nuclear translocator (ARNT). A substrain of Wistar rats, Han/Wistar (Kuopio) (H/W), is about 1000-fold more resistant to the acute lethality of TCDD than other strains, exemplified by Long-Evans (Turku/AB) (L-E); the LD50 values for these two strains are >9600 and 10-20 microg/kg, respectively. Previous studies have demonstrated that the major reason for the exceptional TCDD resistance of H/W rats lies in their AHR, which is remodeled at its C-terminal transactivation domain, but there appears to be another contributing gene product. The present study set out to compare the primary structure of ARNT and the closely related ARNT2 proteins in H/W and L-E rats by cDNA cloning. To our surprise, we found several isoforms of these proteins only one of which has previously been reported in rats. All of the isoforms appeared to arise from alternative splicing. For ARNT, isoforms with deletions at exon 5, 3(') end of exon 6 or 5(') end of exon 11, or with an insertion at 5(') end of exon 20 were discovered. There was also interindividual variation in the number of glutamine-encoding codons at 5(') end of exon 16. The most exciting new variant was revealed for ARNT2, because the insertion found at 5(') end of exon 19 disrupts the functionally critical transactivation domain in the protein, implying a dominant negative role for this isoform. The relative expression levels of the variants did not differ in the two rat strains, nor did TCDD modify the ratios, suggesting that the variants do not contribute to TCDD resistance. However, the regulation of ARNT and ARNT2 activities may be more intricate than previously assumed.     

Expression of the mediators of dioxin toxicity,aryl hydrocarbon receptor (AHR) and the AHR nuclear translocator (ARNT), is developmentally regulated in mouse teeth

Dioxins are persistent and ubiquitous environmental poisons that become enriched in the food chain. Besides being acutely lethal, the most toxic dioxin congener, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is developmentally toxic to many animal species. We have previously found that developing teeth of children may be sensitive to environmental dioxins via their mother's milk and that rat and mouse teeth are dioxin-sensitive throughout their development. The aryl hydrocarbon receptor (AHR) together with the AHR nuclear translocator (ARNT) protein is believed to mediate the toxic effects of dioxins. To study the potential involvement of the AHR-ARNT pathway in the dental toxicity of TCDD, we analysed the expression of AHR and ARNT by in situ hybridization and immunohistochemistry in developing mouse teeth. AHR mRNA first appeared in the epithelium of E12 first molar tooth buds and both proteins were weakly expressed in the bud. After cytodifferentiation the expression was up regulated and became intense in secretory odontoblasts and ameloblasts. The coexpression of AHR and ARNT during early tooth development as well as during the information and mineralization of the dental matrices is suggestive of the AHR-ARNT pathway as a mediator of dental toxicity of TCDD.     

Multicenter evaluation of the novel enzyme immunoassay based on P1-enriched protein for the detection of Mycoplasma pneumoniae infection

The aim of the study was to evaluate new Mycoplasma pneumoniae IgG, IgA and IgM EIA methods based on the enrichment of P1-protein (ThermoLabsystems, Helsinki, Finland) (L) for the detection of acute infection. This evaluation was performed in two independent routine clinical microbiology laboratories. The first laboratory used samples preselected by IgG and IgM Platelia enzyme immunoassay (P) and the second used samples preseleced by Serion ELISA Classic M. pneumoniae IgG, IgM (V). The L method was also compared to the FDA approved method of ImmunoWell M. pneumoniae IgG and IgM (G). When the agreement of two methods was applied as a serologic criteria for an acute infection, the following ratios of acute to nonacute infection were calculated 32/86 (totally 118) in the first and 20/72 (totally 92) in the second laboratory. In the first laboratory, the corresponding ratios by methods were 35/83 (sensitivity 100%, specificity 96.5%), 31/87 (sensitivity 97%, specificity 100%), and 55/63 (sensitivity 100%, specificity 79%) for the L, P and G methods, respectively. In the second laboratory, the ratios were 21/71 (sensitivity 100%, specificity 99%), 16/76 (sensitivity 83%, specificity 100%), and 53/39 (sensitivity 100, specificity 69%) for the L, V and G methods, respectively. Taking into account that the tested sample material was preselected by the P and V methods, which may have introduced some bias in their favor, the newly developed L method utilizing P1-enriched protein was found reliable for serodiagnosis of acute M. pneumoniae infection. The method G was the least specific in detection of acute infection.     

Primary structure and inducibility by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) of aryl hydrocarbon receptor repressor in a TCDD-sensitive and a TCDD-resistant rat strain

The aryl hydrocarbon receptor repressor (AHRR) is a negative regulator of AH receptor (AHR), which mediates most of the toxic and biochemical effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). AHR has been shown to be the major reason for the exceptionally wide (ca. 1000-fold) sensitivity difference in acute toxicity of TCDD between two rat strains, sensitive Long-Evans (Turku/AB) (L-E) and resistant Han/Wistar (Kuopio) (H/W), but there is another, currently unknown contributing factor involved. In the present study, we examined AHRR structure and expression in these rat strains to find out whether AHRR could be this auxiliary factor. Molecular cloning of AHRR coding region showed that consistent with AHRR proteins in other species, the N-terminal end of rat AHRR is highly conserved, but PAS B and Q-rich domains are severely truncated or lacking. Identical structures were recorded in both strains. Next, the time-, dose-, and tissue-dependent expression of AHRR was determined using quantitative real-time RT-PCR. In liver, AHRR expression was very low in untreated rats, but it increased rapidly after TCDD exposure (100microg/kg). Testis exhibited the highest constitutive expression of AHRR, whereas kidney, spleen, and heart showed the highest induction of AHRR in response to TCDD treatment. Again, no marked differences were found between H/W and L-E rats, implying that AHRR is not the auxiliary contributing factor to the strain difference in TCDD sensitivity. However, simultaneous measurement of CYP1A1 mRNA reinforced the view that AHRR is an important determinant of tissue-specific responsiveness to TCDD.     

Regular physical exercise, heart rate variability and turbulence in a 6-year randomized controlled trial in middle-aged men: the DNASCO study

HRV and HRT are independent predictors of cardiovascular mortality. Aging reduces HRV, but results from the physical exercise trials are controversial. The primary aim was to study changes in heart rate variability (HRV) and heart rate turbulence (HRT) in a six-year controlled randomized trial at regular low to moderate intensity physical exercise. One hundred forty men aged 53--63 years were randomized in to an exercise or a control groups. The participants underwent a maximal bicycle ergometer exercise test with respiratory gas analyses annually for six years. At baseline and after intervention, 24-h ambulatory ECG registrations were performed to assess HRV (n=100). HRT was determined among subjects with single ventricular premature complexes (VPC) (n=73). In the exercise group, ventilatory aerobic threshold (VAT) increased by 16% indicating enhanced submaximal cardiorespiratory fitness. No significant differences were found in any of the HRV or HRT parameters between the groups. However, the observed increase in VAT correlated significantly with the improvement in HRV parameters. The change in turbulence slope (TS) correlated with the changes in most HRV variables and the change in turbulence onset (TO) correlated with the changes in three frequency domain parameters. Our results suggest that in addition to improvement in submaximal cardiorespiratory fitness, regular low to moderate intensity physical exercise seems to have beneficial effects also on cardiac autonomic nervous function, a clinically relevant predictor of cardiovascular morbidity and mortality.     

Tumor necrosis factor alpha and ceramide depolarise the resting membrane potential of thyroid FRTL-5 cells via a protein kinase Czeta-dependent regulation of K+ channels

Tumor necrosis factor alpha (TNFalpha) alters the electrophysiological properties of many cell types. In thyroid cells however, the effects have not yet been elucidated. Here, we report the effect of TNFalpha and its second messenger ceramide on the resting membrane potential (RMP) of thyroid FRTL-5 cells. In patch-clamp experiments, we showed that TNFalpha and ceramide depolarise the RMP by inhibiting an acid-sensitive inwardly rectifying potassium current. This depolarisation depended on the activation of protein kinase Czeta (PKCzeta), because it can be blocked by calphostin C, a PKC-inhibitory peptide and a specific inhibitor peptide for PKCzeta. The activation of PKCzeta was confirmed by Western blotting, in which a stimulation with TNFalpha led to the translocation of PKCzeta to the particulate fraction. We conclude that TNFalpha and ceramide depolarise the RMP of thyroid FRTL-5 cells by attenuating a Ba(2+)- and acid-sensitive potassium conductance via activation of PKCzeta.     

Molecular and functional properties of an archaeal phenylalanyl-tRNA synthetase from the hyperthermophile Sulfolobus solfataricus

An archaeal phenylalanyl-tRNA synthetase (FRS) has been purified from the hyperthermophile Sulfolobus solfataricus (Ss). This enzyme is a heterotetramer made of two different subunits whose molecular mass is 56 kDa and 64 kDa, respectively. As thought, SsFRS is essential for the in vitro poly(Phe) synthesis. Interestingly, the enzyme is able to aminoacylate only endogenous tRNA but it does not seem to be a strictly ATP-dependent synthetase. SsFRS interacts with the elongation factor 1alpha isolated from the same source; this caused a significant enhancement of the SstRNA aminoacylation efficiency, thus indicating that, as well as in eukarya, in this archaeon a tRNA channelling mechanism should occur. The overall results presented in this paper show that the archaeal SsFRS behaves as the analogous enzymes isolated from eukaryal sources rather than those from eubacterial organisms.     

Current and Potential Biofuel Production from Plant Oils

Environmental concerns and depletion of fossil fuels along with government policies have led to the search for alternative fuels from various renewable and sustainable feedstocks. This review provides a critical overview of the chemical composition of common commercial plant oils, i.e., palm oil, olive oil, rapeseed oil, castor oil, WCO, and CTO and their recent trends toward potential biofuel production. Plant oils with a high energy content are primarily composed of triglycerides (generally >?95%), accompanied by diglycerides, monoglycerides, and free fatty acids. The heat content of plant oils is close to 90% for diesel fuels. The oxygen content is the most important difference in chemical composition between fossil oils and plant oils. Triglycerides can even be used directly in diesel engines. However, their high viscosity, low volatility, and poor cold flow properties can lead to engine problems. These problems require that plant oils need to be upgraded if they are to be used as a fuel in conventional diesel engines. Biodiesel, biooil, and renewable diesel are the three major biofuels obtained from plant oils. The main constraint associated with the production of biodiesel is the cost and sustainability of the feedstock. The renewable diesel obtained from crude tall oil is more sustainable than biofuels obtained from other feedstocks. The fuel properties of renewable diesel are similar to those of fossil fuels with reduced greenhouse gas emissions. In this review, the chemical composition of common commercial plant oils, i.e., palm oil, olive oil, rapeseed oil, castor oil, and tall oil, are presented. Both their major and minor components are discussed. Their compositions and fuel properties are compared to both fossil fuels and biofuels.     

The key role of extracellular vesicles in the metastatic process

Extracellular vesicles (EVs), including exosomes, have a key role in the paracrine communication between organs and compartments. EVs shuttle virtually all types of biomolecules such as proteins, lipids, nucleic acids, metabolites and even pharmacological compounds. Their ability to transfer their biomolecular cargo into target cells enables EVs to play a key role in intercellular communication that can regulate cellular functions such as proliferation, apoptosis and migration. This has led to the emergence of EVs as a key player in tumor growth and metastasis through the formation of “tumor niches” in target organs. Recent data have also been shown that EVs may transform the microenvironment of primary tumors thus favoring the selection of cancer cells with a metastatic behavior. The release of EVs from resident non-malignant cells may contribute to the metastatic processes as well. However, cancer EVs may induce malignant transformation in resident mesenchymal stem cells, suggesting that the metastatic process is not exclusively due to circulating tumor cells. In this review, we outline and discuss evidence-based roles of EVs in actively regulating multiple steps of the metastatic process and how we can leverage EVs to impair metastasis.