Humpback whale abundance in the North Pacific estimated by photographic capture‐recapture with bias correction from simulation studies

We estimated the abundance of humpback whales in the North Pacific by capture‐recapture methods using over 18,000 fluke identification photographs collected in 2004–2006. Our best estimate of abundance was 21,808 (CV = 0.04). We estimated the biases in this value using a simulation model. Births and deaths, which violate the assumption of a closed population, resulted in a bias of +5.2%, exclusion of calves in samples resulted in a bias of ?10.5%, failure to achieve random geographic sampling resulted in a bias of ?0.4%, and missed matches resulted in a bias of +9.3%. Known sex‐biased sampling favoring males in breeding areas did not add significant bias if both sexes are proportionately sampled in the feeding areas. Our best estimate of abundance was 21,063 after accounting for a net bias of +3.5%. This estimate is likely to be lower than the true abundance due to two additional sources of bias: individual heterogeneity in the probability of being sampled (unquantified) and the likely existence of an unknown and unsampled breeding area (?8.7%). Results confirm that the overall humpback whale population in the North Pacific has continued to increase and is now greater than some prior estimates of prewhaling abundance.     

Piscirickettsia salmonis induces apoptosis in macrophages and monocyte‐like cells from rainbow trout

Piscirickettsia salmonis is the etiologic agent of the salmonid rickettsial septicemia (SRS) which causes significant losses in salmon production in Chile and other and in other regions in the southern hemisphere. As the killing of phagocytes is an important pathogenic mechanism for other bacteria to establish infections in vertebrates, we investigated whether P. salmonis kills trout macrophages by apoptosis. Apoptosis in infected macrophages was demonstrated by techniques based on morphological changes and host cell DNA fragmentation. Transmission electron microcopy showed classic apoptotic characteristics and terminal deoxynucleotidyl transferase‐mediated dUTP nick end labeling showed fragmented DNA. Programmed cell death type I was further confirmed by increased binding of annexin V to externalized phosphatidylserine in infected macrophages. Moreover, significant increases of caspase 3 activation were detected in infected cells and treatment with caspase inhibitor caused a decrease in levels of apoptosis. This is the first evidence that P. salmonis induces cell death in trout macrophages. This could lead to bacterial survival and evasion of the host immune response and play an important role in the establishment of infection in the host. J. Cell. Biochem. 110: 468–476, 2010. © 2010 Wiley‐Liss, Inc.     

Neurogenic differentiation of human adipose-derived stem cells: Relevance of different signaling molecules,transcription factors,and key marker genes

Since numerous diseases affect the central nervous system and it has limited self-repair capability, a great interest in using stem cells as an alternative cell source is generated. Previous reports have shown the differentiation of adipose-derived stem cells in neuron-like cells and it has also been proved that the expression pattern of patterning, proneural, and neural factors, such as Pax6, Mash1, Ngn2, NeuroD1, Tbr2 and Tbr1, regulates and defines adult neurogenesis. Regarding this, we hypothesize that a functional parallelism between adult neurogenesis and neuronal differentiation of human adipose-derived stem cells exists. In this study we differentiate human adipose-derived stem cells into neuron-like cells and analyze the expression pattern of different patterning, proneural, neural and neurotransmitter genes, before and after neuronal differentiation. The neuron-like cells expressed neuronal markers, patterning and proneural factors characteristics of intermediate stages of neuronal differentiation. Thus we demonstrated that it is possible to differentiate adipose-derived stem cells in vitro into immature neuron-like cells and that this process is regulated in a similar way to adult neurogenesis. This may contribute to elucidate molecular mechanisms involved in neuronal differentiation of adult human non-neural cells, in aid of the development of potential therapeutic tools for diseases of the nervous system.     

Anti-Trypanosoma cruzi and cytotoxic activities of Eugenia uniflora L

Chagas disease is caused by Trypanosoma cruzi, being considered a public health problem. An alternative to combat this pathogen is the use of natural products isolated from fruits such as Eugenia uniflora, a plant used by traditional communities as food and medicine due to its antimicrobial and biological activities. Ethanolic extract from E. uniflora was used to evaluate in vitro anti-epimastigote and cytotoxic activity. This is the first record of anti-Trypanosoma activity of E. uniflora, demonstrating that a concentration presenting 50% of activity (EC(50)) was 62.76 μg/mL. Minimum inhibitory concentration (MIC) was ≤ 1024 μg/mL. Our results indicate that E. uniflora could be a source of plant-derived natural products with anti-epimastigote activity with low toxicity.     

Melatonin controls cell proliferation and modulates mitochondrial physiology in pancreatic stellate cells

Journal of Physiology and Biochemistry - We have investigated the effects of melatonin on major pathways related with cellular proliferation and energetic metabolism in pancreatic stellate cells....     

Archaeal and bacterial diversity in five different hydrothermal ponds in the Copahue region in Argentina

Copahue is an acidic geothermal volcanic region in the northwest corner of Neuquén Province, Argentina. In the area, there are various ponds, pools and hot springs with different temperatures, pH values and levels of anthropogenic influence. In this study, the prokaryotic biodiversity of five representative ponds was studied by using two complementary molecular ecology techniques: phylogenetic analysis of 16S rRNA bacterial and archaeal genes and FISH (or CARD-FISH) for quantitative estimation of biodiversity. The results, supported by multivariate statistical analysis, showed that the biodiversity in Copahue ponds seemed to be determined by temperature. High temperature ponds were dominated by archaea, mainly apparently novel representatives from the orders Sulfolobales and Thermoplasmatales that had no close cultivated relatives. By contrast, moderate temperature ponds were colonised by well-characterised sulphur-oxidising bacteria related to acidic environments, such as other geothermal sites or acid mine drainage, and archaea were absent. By combining the biodiversity results from this study and the reported physicochemical features of Copahue, a preliminary model of the possible biogeochemical interaction was outlined for moderate and high temperature ponds.     

Structural basis of pyrrole polymerization in human porphobilinogen deaminase

Human porphobilinogen deaminase (PBGD), the third enzyme in the heme pathway, catalyzes four times a single reaction to convert porphobilinogen into hydroxymethylbilane. Remarkably, PBGD employs a single active site during the process, with a distinct yet chemically equivalent bond formed each time. The four intermediate complexes of the enzyme have been biochemically validated and they can be isolated but they have never been structurally characterized other than the apo- and holo-enzyme bound to the cofactor. We present crystal structures for two human PBGD intermediates: PBGD loaded with the cofactor and with the reaction intermediate containing two additional substrate pyrrole rings. These results, combined with SAXS and NMR experiments, allow us to propose a mechanism for the reaction progression that requires less structural rearrangements than previously suggested: the enzyme slides a flexible loop over the growing-product active site cavity. The structures and the mechanism proposed for this essential reaction explain how a set of missense mutations result in acute intermittent porphyria.     

Involvement of the pyrophosphate and the 2'-phosphate binding regions of ferredoxin-NADP+ reductase in coenzyme specificity

Previous studies indicated that the determinants of coenzyme specificity in ferredoxin-NADP+ reductase (FNR) from Anabaena are situated in the 2'-phosphate (2'-P) NADP+ binding region, and also suggested that other regions must undergo structural rearrangements of the protein backbone during coenzyme binding. Among the residues involved in such specificity could be those located in regions where interaction with the pyrophosphate group of the coenzyme takes place, namely loops 155-160 and 261-268 in Anabaena FNR. In order to learn more about the coenzyme specificity determinants, and to better define the structural basis of coenzyme binding, mutations in the pyrophosphate and 2'-P binding regions of FNR have been introduced. Modification of the pyrophosphate binding region, involving residues Thr-155, Ala-160, and Leu-263, indicates that this region is involved in determining coenzyme specificity and that selected alterations of these positions produce FNR enzymes that are able to bind NAD+. Thus, our results suggest that slightly different structural rearrangements of the backbone chain in the pyrophosphate binding region might determine FNR specificity for the coenzyme. Combined mutations at the 2'-P binding region, involving residues Ser-223, Arg-224, Arg-233, and Tyr-235, in combination with the residues mentioned above in the pyrophosphate binding region have also been carried out in an attempt to increase the FNR affinity for NAD+/H. However, in most cases the analyzed mutants lost the ability for NADP+/H binding and electron transfer, and no major improvements were observed with regard to the efficiency of the reactions with NAD+/H. Therefore, our results confirm that determinants for coenzyme specificity in FNR are also situated in the pyrophosphate binding region and not only in the 2'-P binding region. Such observations also suggest that other regions of the protein, yet to be identified, might also be involved in this process.     

First Report of Peronospora belbahrii on Sweet Basil in Baja California Sur,México

In Baja California Sur, Mexico, a foliar disease occurred on sweet basil which seriously affected its quality and yield. The most common symptoms were yellowing and necrosis on leaves, caused by a downy mycelium growth on the lower leaf surface. Symptomatic leaves from two sampling sites were collected for morphological studies and molecular analysis of pathogen DNA. Based on morphological characteristics (sporangiophore size of 240–530 × 7–11 μm, branches of 5–8 order and a sporangia size of 27–31 × 21–25 μm) and molecular analysis (the GenBank blast of the PCR assays showed unique rDNA sequence data with 99% similarity to P. belbahrii), the pathogen was identified as Peronospora belbahrii, the causal agent of basil downy mildew. This is the first report of P. belbahrii affecting sweet basil in Mexico.