![[PukiWiki]](image/pukiwiki.png "[PukiWiki]")
#author("2024-12-07T07:49:25+09:00","","") Karenia selliformis is a bloom-forming toxic dinoflagellate known for production of gymnodimines (GYMs) and causing mass mortalities of marine fauna. Blooms have been reported from coastal waters of New Zealand, Mexico, Tunisia, Kuwait, Iran, China and Chile. Based on molecular phylogeny, morphology, toxin production, pigment composition and cell growth of Chilean K. selliformis isolated in 2018 (CREAN_KS01 and CREAN_KS02), this study revealed a more complex diversity within this species than previously thought. A phylogenetic reconstruction based on the large sub-unit ribosomal nucleotide (LSU rDNA) and Internal Transcriber Spacer (ITS) sequences of 12 worldwide isolates showed that within the K. selliformis clade there are at least two different phylotypes with clear phenotypic differences. Morphological differences related to the dorsal-ventral compression, shape of the hyposome and the presence of pores on the left lobe of the hyposome. A comparison of pigment signatures among worldwide isolates revealed ummer season. In conclusion, the present study provides evidence for significant genetic and phenotypic variability among worldwide isolates, which points to the existence of a K. selliformis "species complex". The massive fauna mortality during K. selliformis bloom events in the Chilean coast cannot be explained by GYMs nor brevetoxins, but can to a large extent be accounted for by the high production of long-chain PUFAs and/or still uncharacterized highly toxic compounds.Raphidiopsis raciborskii is a freshwater, potentially toxigenic cyanobacterium, originally described as a tropical species that is spreading to northern regions over several decades. The ability of R. raciborskii to produce cyanotoxins - in particular the alkaloid cylindrospermopsin (CYN), which is toxic to humans and animals - is of serious concern. The first appearance of R. raciborskii in Russia was noted in Lake Nero in the summer of 2010. This is the northernmost (57°N) recorded case of the simultaneous presence of R. raciborskii and detection of CYN. In this study, the data from long-term monitoring of the R. raciborskii population, temperature and light conditions in Lake Nero were explored. CYN and cyr/aoa genes present in environmental samples were examined using HPLC/MS-MS and PCR analysis. A R. raciborskii strain (R104) was isolated and its morphology, toxigenicity and phylogeography were studied. It is supposed that the trigger factor for the strong development of R. raciborskii in Lake Nero in suins isolated from very remote continents might be related to the ancient origin of the cyanobacterium inhabiting the united continents of Laurasia and Gondwana, rather than comparably recent transoceanic exchange between R. raciborskii populations.Blooms of harmful algae are increasing globally, yet their impacts on copepods, an important link between primary producers and higher trophic levels, remain largely unknown. Algal toxins may have direct, negative effects on the survival of copepods. They may also indirectly affect copepod survival by deterring feeding and thus decreasing the availability of energy and nutritional resources. Here we present a series of short-term (24 h) experiments in which the cosmopolitan marine copepod, Acartia tonsa, was exposed to a range of concentrations of the toxic dinoflagellate, Alexandrium catenella (strain 1119/27, formerly Alexandrium tamarense), with and without the presence of alternative, non-toxic prey (Rhodomonas sp.). We also present the toxin profile concentrations for A. https://www.selleckchem.com/products/mitomycin-c.html catenella. The survival and feeding of A. tonsa were not affected across the range of concentrations recorded for A. catenella in the field; increased mortality of A. tonsa was only discernible when A. catenella was present at concentrations that exceed their reported environmental concentrations by two orders of magnitude. The observed lethal median concentration (LC50) for A. tonsa exposed to A. catenella was 12.45 ng STX eq L-1. We demonstrate that A. tonsa is capable of simultaneously ingesting both toxic and non-toxic algae, but increases clearance rates towards non-toxic prey as the proportional abundance of toxic A. catenella increases. The ability to actively select non-toxic algae whilst also ingesting toxic algae suggests that consumption of the latter does not cause physical incapacitation and thus does not affect ingestion in A. tonsa. This work shows that short-term exposure to toxic A. catenella is unlikely to elicit major effects on the grazing or survival of A. tonsa. However, more work is needed to understand the longer-term and sub-lethal effects of toxic algae on marine copepods.Human lactoferrin (hLF) is a glycosaminoglycan (GAG)-binding protein involved in various biological functions. It consists of two globular functional domains, referred to as the N- and C-lobes. Both heparin (HP) and heparan sulfate (HS) bind to the N-lobe domain of hLF. Although some biological functions of hLF such as neuroprotective effects and cancer growth inhibition are regulated by its binding to HS, the binding characteristics of hLF with other GAG subtypes, and their effects on biological activities are still poorly understood. Here, we report that hLF binds to chondroitin sulfate (CS)-E, a GAG subtype involved in various neurodegenerative diseases. The α-helical content of hLF, which is an indicator of changes in the secondary structure of hLF, increased in the presence of CS-C, CS-D, or CS-E, but not in the presence of HP, HS, CS-A, or CS-B. This structural change was also observed in the N-lobe, the N-terminal half region of the hLF. Additionally, the thermal stability of the N-lobe showed a dose-dependent improvement in the presence of CS-E, but not in the presence of HP. This indicates that the binding mode of hLF/N-lobe to CS-E may differ from that of HP. hLF was also found to neutralize CS-E-induced inhibition of neurite outgrowth and neuronal growth cone collapse, which are neurodegenerative responses to spinal cord injury, in cultured dorsal root ganglion neurons. Thus, hLF is a promising drug candidate for the treatment of CS-E-induced neurodegenerative diseases such as spinal cord injury.
