Even though Mussolini’s famous definition of cinema as “the strongest weapon” implies a common ground between filmmaking, propaganda, technology, and warfare, a casual viewer of Fascist-era films would be hard-pressed to find explicit references to this interconnectedness. In fact, narrative films made at the time hardly ever dealt with the realities of the regime, to the point that in 1979 Carlo Lizzani spoke of Fascist cinema by calling it “an absence.” Nonetheless, the Fascist obsession with modernity and technological innovations emerges in different ways from most films produced during the Ventennio. Despite their surface-level optimism and faith in the process of modernization, many of these films betray the feelings of anxiety and uncertainty that accompanied the shift from tradition to modernity, reflecting the complexity of the regime’s own attitude towards these cultural modes. In particular, films shot on location in the colonial territories of Eastern Africa display an interesting ambivalence towards technology and the colonial effort itself: while their narratives are seemingly celebratory, the cinematic style they display reveals a more complicated relationship with the Fascist myth-making agenda.

This paper will examine four titles belonging to this body of films, grouped by Ruth Ben-Ghiat under the label of Fascism’s Empire Cinema, and will explore their portrayal of modernity by focusing on their representation of the relationship between technology and the human body. I will argue that these films reflect the contradictions intrinsic to the Fascist ideology of progress, and the technological mediation of the camera allows for this ambivalence to emerge without being explicitly stated. That is why, rather than adopting a cultural studies approach, I will employ film analysis as a tool to conduct historical research. I will depart from the film texts and, by analyzing the formal structure of some of their key moments, will locate the places in which feelings of uncertainty towards Fascist ideals of progress, strength, and masculinity ripple underneath a seemingly triumphal surface.

Polypeptide materials were developed to address a variety of biomedical applications, including tissue engineering and drug delivery. This work was focused on increasing the pool of amino acid monomers to further the functionality and manipulation of polypeptide materials. This dissertation describes the development of polypeptide materials with stimuli-responsive behaviors and new functionality.

A boronic acid-functionalized polypeptide-PEG copolymer was synthesized. This copolymer demonstrated the ability to reversibly bind to glycosylated enzymes; formed stable complexes at pH 7.4, and dissociated at pH 5.0, the pH of a lysosomal compartment. This complexation was specific to glycosylated enzymes and the boronic acid functionality used. These results suggest potential application of these copolymers in enzyme replacement therapies.

A new L-lysine based -amino acid N-carboxyanhydride (NCA) monomer was synthesized in order to prepare photodegradable polypeptide hydrogels. The lysine derivative was caged using a UV-labile protecting group. Hydrogels were assembled using this residue as the hydrophobic block. Material properties could be adjusted by variation of hydrophobic block length and composition, as well as polymer concentration in water. These parameters were also used to tune the degradation profile of these hydrogels upon exposure to 365 nm light. Loading of dyes into these networks followed by irradiation demonstrated the ability for these gels to encapsulate and facilitate the triggered release of therapeutics.

Finally, polysulfonium-based polypeptide hydrogels were synthesized, assembled and characterized using unnatural amino acid NCA monomers. Creation of these new materials relied on application of previously reported post-polymerization thioether alkylation methodology from the Deming lab to new building blocks. The resulting polymers were found to tolerate a range of functionality without loss of hydrogel properties. While hydrophobic block length and polymer concentration were used to tune gel properties, the choice of alkylating agent was also responsible for changing gel stiffness. Use of mixtures of different alkylating agents led to further fine adjustment of materials properties. The incorporation of azide groups was also tolerated by the scaffolds, and this functionality was used for subsequent click chemistry to demonstrate the retention of gel properties even after further functionalization. This methodology has implications for the incorporation of fluorescent labels or cell attachment-promoting ligands.

Acoustic waves below the audible frequencies (20 Hz) are called infrasound. Generated by a wide variety of sources, these signals can propagate thousands of kilometers, aided by their low attenuation as well as strong winds and high temperatures in the stratosphere and thermosphere that enable them to return to the ground. Volcanic eruptions are among the most powerful sources of infrasound, and the International Monitoring System (IMS) infrasound network, maintained by the Comprehensive Nuclear-Test-Ban Treaty Organization (CTBTO), is capable of monitoring volcanic eruptions around theglobe. However, the spatiotemporal variability of the atmosphere poses a major challenge. In particular, strong horizontal cross-winds affect the observed infrasound arrival back-azimuths, causing source mislocations up to hundreds of kilometers. This dissertation presents an automatic iterative method combining empirical climatologies (HWM14/NRLMSIS2.0) and 3D ray tracing (infraGA) to obtain rapid, robust first-order estimates of the back-azimuth deviations, producing corrections for location and characterization procedures. The results compare well with a more realistic model of the lower atmosphere using Numerical Weather Prediction (NWP) simulations. Potential applications include near real-time volcano monitoring and large-scale reanalysis of infrasound archives. To test this method, we first apply it to the eruptions of Puyehue-Cordón Caulle (2011) and Calbuco (2015) in Chile, using data from IMS stations within 5000 km. The back-azimuth corrections reduce the source mislocation by ∼84% (242 to 38.7 km) and ∼75% (366 to 93.1 km), respectively. Then, we assess the method’s temporal accuracy using data from 2003-2022 from IMS station IS22 (New Caledonia), which has recorded persistent volcanic infrasound from Yasur (∼400 km) and Ambrym (∼700 km) volcanoes (Vanuatu archipelago). We find good agreement with the seasonal variation of the dataset, showing we can provide year-long estimates of the back-azimuth deviation. Finally, we use the method to identify long-range infrasound signals recorded at the Antarctic IMS station IS27, attributable to episodes of moderate persistent eruptive activity at Mount Michael volcano, 1,670 km away on Saunders island (South Sandwich islands). Examining data from 2004-2020 reveals previously hidden candidate eruptive signals, especially from May 2005 to January 2008 and from May 2016 to April 2018.

Intoxication with organophosphate (OP) acetylcholinesterase inhibitors represent a chemical threat and a global public health issue. Acute OP intoxication triggers a cholinergic crisis that can progress to seizures, status epilepticus (SE) and death. Current standard of care increases the survival rate of patients acutely intoxicated with OPs, but does not prevent long-term neurological sequelae, specifically, epilepsy and cognitive impairment. SE induced by etiologies other than OP intoxication similarly progress to long-term adverse neurological consequences, and to date there are no effective therapeutic strategies for these situations either. Progress in addressing this clinical gap has been stymied by significant data gaps regarding the pathogenic mechanism(s) underlying the persistent neurological consequences associated with acute SE. Predominant hypothesis include neuroinflammation, oxidative stress and/or damage to the blood-brain barrier (BBB). The BBB is vital for the maintenance of a regulated brain milieu required for normal neurological function; the BBB also protects brain cells from toxic blood-borne compounds. BBB impairment has been reported following acute OP-induced SE and SE caused by other etiologies. A dysfunctional BBB has also been documented in patients with epilepsy and cognitive deficits. It is hypothesized that BBB disruption is involved in the pathogenesis of epilepsy and cognitive impairment, and, therefore, stabilization of the BBB following acute SE could mitigate such neuropathologies. This dissertation focuses on characterizing the disruption of the BBB following OP-induced SE using a rat model of acute intoxication with the OP diisopropylfluorophosphate (DFP). It further seeks to determine whether repurposing Cmpd10357, a drug that targets the plasminogen activating system (PAS), mitigates BBB dysfunction in rats acutely intoxicated with DFP.Chapter 2 identified breach of the BBB as determined by contrast MRI and immunohistochemical localization of serum albumin in the brain parenchyma as early as 6 h post-exposure in the piriform cortex (PRC) and amygdala (AMY) of male rats and remained severe until 7 days post-exposure (DPE). This BBB leakiness was mild to moderate and transient in the thalamus, hippocampus and somatosensory cortex. Chapter 3 characterized the spatiotemporal profile of OP-induced BBB instability in the PRC and AMY of male and female rats, observing a leakage of sodium fluorescein, MRI contrast and serum albumin that persisted up to 28 DPE. Female rats presented less severe signs of BBB dysfunction when inspected by MRI. The components of the neurovascular unit (NVU) were examined and general dysregulation of all elements of the NVU were evident by 3 to 7 DPE and persisted up to 28 DPE. Chapter 3 also revealed that the BBB dysfunction post-DFP poisoning is SE-dependent, and occurs largely independent of OP-induced cholinergic crisis. Lastly, chapter 4 showed Cmpd10357 is ineffective in protecting the BBB in rats acutely intoxicated with DFP. There were no differences in serum albumin leakage in the PRC and AMY of DFP-intoxicated rats treated with this drug vs. those that were not treated. Interestingly, treatment with Cmpd10357 also had no effect on the expression of tissue and urokinase plasminogen activators (tPA and uPA), or the count of astrocytes expressing plasminogen activator inhibitor 1 (PAI-1). In conclusion, the findings of this dissertation strengthen the hypothesis that BBB disruption is associated with long-term neurological consequences of acute OP-induced SE. These data provide insight regarding a temporal window for administration of therapeutics to stabilize the BBB, potential biomarkers for quantifying effectiveness of these therapies, and even novel therapeutic targets. In addition, the results presented here enhance the translatability of data generated from the rat acute model of DFP intoxication to other models of SE and, to some extent, to clinical settings. Lastly, the lack of therapeutic efficacy of Cmpd10357 suggests that mechanistically different PAS-targeting drugs be considered for stabilizing the BBB post-DFP intoxication.