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"Nanni, Giordano"
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The ʹMinutes of Evidenceʹ project
The preceding chapters of this collection demonstrate how nuanced and critically informed analyses of historical evidence can deepen and refine our understanding of nineteenth-century Victorian society. In this chapter, we seek a similar outcome; but we shift the focus towards the task of using historical materials to engage a broader public audience. In doing so we consider the potential benefits of expanding the field of engagement with the past through an innovative collaboration which aims to bring Victoria’s history ‘back to life’ through theatre; by (re)citing its historical archive, and taking the words ‘off the page’ and voicing them out
Book Chapter
Fascinating history brought to life
A little-known true story about a short-lived revolutionary experiment in Aboriginal self-determination formed the basis for the play Coranderrk, which is on at the Playhouse for two nights only on ...
Newspaper Article
The Colonisation of Time: Ritual, Routine, and Resistance in the British Empire
McKenzie reviews The Colonisation of Time: Ritual, Routine, and Resistance in the British Empire by Giordano Nanni.
Book Review
Hunting and Habitat Destruction Drive Widespread Functional Declines of Top Predators in a Global Deforestation Hotspot
Aim We investigated the effects of habitat destruction and hunting on the functional decline of top predators, specifically jaguar and puma, in the Gran Chaco. Location The 1.1 million km2 South American Gran Chaco. Methods We used spatially explicit, individual‐based models for jaguars and pumas, incorporating detailed information on habitat suitability and hunting pressure. We parameterized our models with literature data and calibrated them through a Delphi expert‐elicitation process. We simulated population trajectories under a hypothetical, threat‐free, baseline versus different threat scenarios. Results Under combined threats of hunting and habitat loss, jaguar and puma populations declined by 88% and 80%, respectively, compared to range contractions of 48% and 35%, respectively. Both species remained regionally viable, particularly due to large protected areas, which acted as population sources but were surrounded by strong sinks. We observed a widespread weakening of the top carnivore guild function, with at least one species extirpated across 67% of the Chaco and strong declines (> 80%; considered here as functional loss) for both species concurrently across 61% of their area of historical co‐occurrence. Hunting was a much stronger driver of population declines (88% and 77% for jaguars and pumas, respectively) compared to habitat destruction (26% and 22%). Main Conclusions Large predators play key functional roles in ecosystems. Our findings reveal that these functions can be lost over vast areas due to the combined effects of habitat destruction and hunting, with functional loss extending far beyond the areas of species' extirpation. Very large protected areas, like Kaa‐Iya in Bolivia, are crucial for maintaining viable populations of top predators, highlighting the pressing need for increased protection and connectivity in the Chaco to prevent further trophic downgrading. More generally, our research underscores the value of spatially detailed, mechanistic models for disentangling the complex dynamics of multiple threats on ecological functioning at broad scales.
Journal Article
Bone sarcoma patient-derived xenografts are faithful and stable preclinical models for molecular and therapeutic investigations
Standard therapy of osteosarcoma (OS) and Ewing sarcoma (EW) rests on cytotoxic regimes, which are largely unsuccessful in advanced patients. Preclinical models are needed to break this impasse. A panel of patient-derived xenografts (PDX) was established by implantation of fresh, surgically resected osteosarcoma (OS) and Ewing sarcoma (EW) in NSG mice. Engraftment was obtained in 22 of 61 OS (36%) and 7 of 29 EW (24%). The success rate in establishing primary cell cultures from OS was lower than the percentage of PDX engraftment in mice, whereas the reverse was observed for EW; the implementation of both
in vivo
and
in vitro
seeding increased the proportion of patients yielding at least one workable model. The establishment of
in vitro
cultures from PDX was highly efficient in both tumor types, reaching 100% for EW. Morphological and immunohistochemical (SATB2, P-glycoprotein 1, CD99, caveolin 1) studies and gene expression profiling showed a remarkable similarity between patient’s tumor and PDX, which was maintained over several passages in mice, whereas cell cultures displayed a lower correlation with human samples. Genes differentially expressed between OS original tumor and PDX mostly belonged to leuykocyte-specific pathways, as human infiltrate is gradually replaced by murine leukocytes during growth in mice. In EW, which contained scant infiltrates, no gene was differentially expressed between the original tumor and the PDX. A novel therapeutic combination of anti-CD99 diabody C7 and irinotecan was tested against two EW PDX; both drugs inhibited PDX growth, the addition of anti-CD99 was beneficial when chemotherapy alone was less effective. The panel of OS and EW PDX faithfully mirrored morphologic and genetic features of bone sarcomas, representing reliable models to test therapeutic approaches.
Journal Article
Evolution of HER2-positive mammary carcinoma: HER2 loss reveals claudin-low traits in cancer progression
HER2-positive breast cancers may lose HER2 expression in recurrences and metastases. In this work, we studied cell lines derived from two transgenic mammary tumors driven by human HER2 that showed different dynamics of HER2 status. MamBo89HER2stable cell line displayed high and stable HER2 expression, which was maintained upon in vivo passages, whereas MamBo43HER2labile cell line gave rise to HER2-negative tumors from which MamBo38HER2loss cell line was derived. Both low-density seeding and in vitro trastuzumab treatment of MamBo43HER2labile cells induced the loss of HER2 expression. MamBo38HER2loss cells showed a spindle-like morphology, high stemness and acquired in vivo malignancy. A comprehensive molecular profile confirmed the loss of addiction to HER2 signaling and acquisition of an EMT signature, together with increased angiogenesis and migration ability. We identified PDGFR-B among the newly expressed determinants of MamBo38HER2loss cell tumorigenic ability. Sunitinib inhibited MamBo38HER2loss tumor growth in vivo and reduced stemness and IL6 production in vitro. In conclusion, HER2-positive mammary tumors can evolve into tumors that display distinctive traits of claudin-low tumors. Our dynamic model of HER2 status can lead to the identification of new druggable targets, such as PDGFR-B, in order to counteract the resistance to HER2-targeted therapy that is caused by HER2 loss.
Journal Article