Island and Mountain Ecosystems as Testbeds for Biological Control in the Anthropocene

For centuries, islands and mountains have incited the interest of naturalists, evolutionary biologists and ecologists. Islands have been the cradle for biogeography and speciation theories, while mountain ranges have informed how population adaptation to thermal floors shapes the distribution of species globally. Islands of varying size and mountains’ altitudinal ranges constitute unique “natural laboratories” where one can investigate the effects of species loss or global warming on ecosystem service delivery. Although invertebrate pollination or seed dispersal processes are steadily being examined, biological control research is lagging. While observations of a wider niche breadth among insect pollinators in small (i.e., species-poor) islands or at high (i.e., colder) altitudes likely also hold for biological control agents, such remains to be examined. In this Perspective piece, we draw on published datasets to show that island size alone does not explain biological control outcomes. Instead, one needs to account for species’ functional traits, habitat heterogeneity, host community make-up, phenology, site history or even anthropogenic forces. Meanwhile, data from mountain ranges show how parasitism rates of Noctuid moths and Tephritid fruit flies exhibit species- and context-dependent shifts with altitude. Nevertheless, future empirical work in mountain settings could clarify the thermal niche space of individual natural enemy taxa and overall thermal resilience of biological control. We further discuss how global databases can be screened, while ecological theories can be tested, and simulation models defined based upon observational or manipulative assays in either system. Doing so can yield unprecedented insights into the fate of biological control in the Anthropocene and inform ways to reinforce this vital ecosystem service under global environmental change scenarios.The development of this manuscript was funded by the Food and Agriculture Organization FAO through LOA/RAP/2021/57, executed by The University of Queensland. AS was supported by the "Ramon y Cajal" program (RYC2020029407-I), financed by the Spanish "Ministerio de Ciencia e Innovacion".info:eu-repo/semantics/publishedVersio

Correlation between the progressive cytoplasmic expression of a novel small heat shock protein (Hsp16.2) and malignancy in brain tumors

<p>Abstract</p> <p>Background</p> <p>Small heat shock proteins are molecular chaperones that protect proteins against stress-induced aggregation. They have also been found to have anti-apoptotic activity and to play a part in the development of tumors. Recently, we identified a new small heat shock protein, Hsp16.2 which displayed increased expression in neuroectodermal tumors. Our aim was to investigate the expression of Hsp16.2 in different types of brain tumors and to correlate its expression with the histological grade of the tumor.</p> <p>Methods</p> <p>Immunohistochemistry with a polyclonal antibody to Hsp16.2 was carried out on formalin-fixed, paraffin-wax-embedded sections using the streptavidin-biotin method. 91 samples were examined and their histological grade was defined. According to the intensity of Hsp16.2 immunoreactivity, low (+), moderate (++), high (+++) or none (-) scores were given.</p> <p>Immunoblotting was carried out on 30 samples of brain tumors using SDS-polyacrylamide gel electrophoresis and Western-blotting.</p> <p>Results</p> <p>Low grade (grades 1–2) brain tumors displayed low cytoplasmic Hsp16.2 immunoreactivity, grade 3 tumors showed moderate cytoplasmic staining, while high grade (grade 4) tumors exhibited intensive cytoplasmic Hsp16.2 staining. Immunoblotting supported the above mentioned results. Normal brain tissue acted as a negative control for the experiment, since the cytoplasm did not stain for Hsp16.2. There was a positive correlation between the level of Hsp16.2 expression and the level of anaplasia in different malignant tissue samples.</p> <p>Conclusion</p> <p>Hsp16.2 expression was directly correlated with the histological grade of brain tumors, therefore Hsp16.2 may have relevance as becoming a possible tumor marker.</p

TRPA1 is essential for the vascular response to environmental cold exposure

This work was supported by the British Heart Foundation and a Capacity Building Award in Integrative Mammalian Biology. It was also supported by Arthritis Research UK and XK is supported by a British Pharmacological Society AJ Clark studentship

The Inhibitory Effect of a Novel Cytotoxic Somatostatin Analogue AN-162 on Experimental Glioblastoma

Abstract Glioblastoma multiforme is the most common and most aggressive type of high grade tumor with a poor prognosis upon discovery. Based on earlier promising results earned with AN-162, a doxorubicin molecule linked to somatostatin (SST) analogue RC-160, it was our aim to determine the effect of AN-162 on DBTRG-05 glioblastoma cell line, and to test its efficacy in experimental brain tumors. We detected the expression of mRNA for somatostatin receptor (SSTR) subtypes 2 and 3 in DBTRG-05 cells with RT-PCR. Using ligand competition assay, specific high affinity receptors for somatostatin were found. The MTT assay showed that both AN-162 and doxorubicin (DOX) significantly inhibited cell proliferation and that there was no significant difference between the effects in vitro. Nude mice were xenografted with DBTRG-05 glioblastoma tumors. AN-162 showed a significant inhibition of tumor growth compared with the control group and the groups treated with equimolar doses of doxorubicin, somatostatin analogue RC-160, or the unconjugated mixture of doxorubicin plus RC-160. The tumor doubling time in the group of animals treated with AN-162 was extended and was significantly different from doubling times in the control group and in the other treatment groups. Our study clearly demonstrates a potent inhibitory effect of AN-162 in experimental glioblastoma, thus suggesting the possibility of its utilization in patients suffering from malignant brain cancer