Bushfire catastrophe in Victoria, Australia : public record, accountability, commemoration, memorialization and heritage protection

In Australia, 7 February 2009 has become known as ‘Black Saturday’ because of the bushfire catastrophe that took 173 lives and devastated communities in the central parts of the State of Victoria. The paper considers how the 2009 fires have been recorded, how the issue of accountability has been dealt with, particularly in relation to the State and its agencies but also individual residents in the fire-devastated areas, and how bushfire deaths and other losses have been commemorated through remembrance events and museum collection projects and memorialized through the creation of new monuments and the protection of remaining physical structures as official heritage. Despite the major impact of bushfires on the State, to date few bushfire-related places have been protected. The former Cockatoo Kindergarten, which acted as a community refuge during an earlier catastrophic Victorian bushfire on Ash Wednesday, 16 February 1983, is an exception. Inscribed in 2012, the former kindergarten is the only bushfire-related place inscribed on the Victorian Heritage Register, in this case for its historical and social value as a place resonating with other communities affected by other bushfires and helping the broader Victorian public to come to terms with bushfire catastrophe. But, while bushfire commemoration activities and physical memorials, like those relating to war, help many societies remember individual and community pain and suffering, they can divert attention from the more fundamental questions of why they were there in the first place and what must be done to ensure the same catastrophe does not recur in the future. In this regard, the paper questions the oft-cited claim that bushfires are embedded in the Australian psyche, seeing links between the rhetoric around bushfire survival and Australian myth-making and nation-building.

The Ca2+-activated K+ channels play a braking role in locus coeruleus neurons during CO2 exposure

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

[The abdominal catastrophe]

Patients with an abdominal catastrophe are in urgent need of early, interdisciplinary medical help. The treatment plan should be based on medical priorities and clear leadership. First priority should be given to achieve optimal oxygenation of blood and stabilization of circulation during all treatment-phases. The sicker the patient, the less invasive the (surgical) treatment should to be, which means "damage control only". This short article describes 7 important, pragmatic rules that will help to increase the survival of a patient with an abdominal catastrophe. Preexisting morbidity and risk factors must be included in the overall risk-evaluation for every therapeutic intervention. The challenge in patients with an abdominal catastrophe is to carefully balance the therapeutic stress and the existing resistance of the individual patient. The best way to avoid abdominal disaster, however, is its prevention.

ATG5 is induced by DNA-damaging agents and promotes mitotic catastrophe independent of autophagy

Anticancer drug therapy activates both molecular cell death and autophagy pathways. Here we show that even sublethal concentrations of DNA-damaging drugs, such as etoposide and cisplatin, induce the expression of autophagy-related protein 5 (ATG5), which is both necessary and sufficient for the subsequent induction of mitotic catastrophe. We demonstrate that ATG5 translocates to the nucleus, where it physically interacts with survivin in response to DNA-damaging agents both in vitro and in carcinoma tissues obtained from patients who had undergone radiotherapy and/or chemotherapy. As a consequence, elements of the chromosomal passenger complex are displaced during mitosis, resulting in chromosome misalignment and segregation defects. Pharmacological inhibition of autophagy does not prevent ATG5-dependent mitotic catastrophe, but shifts the balance to an early caspase-dependent cell death. Our data suggest a dual role for ATG5 in response to drug-induced DNA damage, where it acts in two signalling pathways in two distinct cellular compartments, the cytosol and the nucleus.

Histoire édifiante et curieuse de Rothschild Ier, roi de Juifs : suivie du récit de la catastrophe du 8 Juillet

par un témoin coulaire

Nouvelle réponse du prince des Israélites Rothschild Ier a un pamphlétaire : suivie d'une dissertation sur la catastrophe du 8 juillet

par M. P. de R. ...

Driving and emergency braking may be impaired after tibiotalar joint arthrodesis: conclusions after a case series.

PURPOSE To assess whether reaction time (RT) and movement time (MT), as the two components of the total brake response time (TBRT) and brake force (BF) are different in patients with a foot joint arthrodesis in comparison to controls. METHODS The study was a comparative case series in a driving simulator under realistic driving conditions. Mobile patients without a walker, ≥6 months after surgery who were driving a car and had no neurological co-morbidity, knee or hip joint prosthesis were included in the study. The selection criteria resulted in 12 patients with right tibiotalar joint arthrodesis (TTJA) and 12 patients with another right foot joint arthrodesis (OFJA), who were compared to 17 individuals without any ankle-joint pathology. For TBRT, an empirical safe driving threshold of 700 ms was used. The outcome measures were RT, MT, TBRT, BF and McGuire score. RESULTS MT (p = 0.034) and TBRT (p = 0.026) were longer in TTJA patients in comparison with the controls. Also, more patients with TTJA than patients with OFJA and controls exceeded the safe driving threshold (p = 0.028). The outcomes in OFJA patients and in controls were comparable. The McGuire score was similar between the TTJA and OFJA patients (p = 0.26). CONCLUSIONS Significantly slower MT and TBRT, and significantly more patients exceeding the safe driving threshold, were observed after a tibiotalar-joint arthrodesis in comparison to the controls. Patients with OFJAs were not significantly different from the controls. Driving and emergency braking may be impaired after tibiotalar-joint arthrodesis.

Making Transport Safer: V2V-Based Automated Emergency Braking System

An important goal in the field of intelligent transportation systems (ITS) is to provide driving aids aimed at preventing accidents and reducing the number of traffic victims. The commonest traffic accidents in urban areas are due to sudden braking that demands a very fast response on the part of drivers. Attempts to solve this problem have motivated many ITS advances including the detection of the intention of surrounding cars using lasers, radars or cameras. However, this might not be enough to increase safety when there is a danger of collision. Vehicle to vehicle communications are needed to ensure that the other intentions of cars are also available. The article describes the development of a controller to perform an emergency stop via an electro-hydraulic braking system employed on dry asphalt. An original V2V communication scheme based on WiFi cards has been used for broadcasting positioning information to other vehicles. The reliability of the scheme has been theoretically analyzed to estimate its performance when the number of vehicles involved is much higher. This controller has been incorporated into the AUTOPIA program control for automatic cars. The system has been implemented in Citroën C3 Pluriel, and various tests were performed to evaluate its operation.

Dissociation of the Tubulin-sequestering and Microtubule Catastrophe-promoting Activities of Oncoprotein 18/Stathmin

Oncoprotein 18/stathmin (Op18) has been identified recently as a protein that destabilizes microtubules, but the mechanism of destabilization is currently controversial. Based on in vitro microtubule assembly assays, evidence has been presented supporting conflicting destabilization models of either tubulin sequestration or promotion of microtubule catastrophes. We found that Op18 can destabilize microtubules by both of these mechanisms and that these activities can be dissociated by changing pH. At pH 6.8, Op18 slowed microtubule elongation and increased catastrophes at both plus and minus ends, consistent with a tubulin-sequestering activity. In contrast, at pH 7.5, Op18 promoted microtubule catastrophes, particularly at plus ends, with little effect on elongation rates at either microtubule end. Dissociation of tubulin-sequestering and catastrophe-promoting activities of Op18 was further demonstrated by analysis of truncated Op18 derivatives. Lack of a C-terminal region of Op18 (aa 100–147) resulted in a truncated protein that lost sequestering activity at pH 6.8 but retained catastrophe-promoting activity. In contrast, lack of an N-terminal region of Op18 (aa 5–25) resulted in a truncated protein that still sequestered tubulin at pH 6.8 but was unable to promote catastrophes at pH 7.5. At pH 6.8, both the full length and the N-terminal–truncated Op18 bound tubulin, whereas truncation at the C-terminus resulted in a pronounced decrease in tubulin binding. Based on these results, and a previous study documenting a pH-dependent change in binding affinity between Op18 and tubulin, it is likely that tubulin sequestering observed at lower pH resulted from the relatively tight interaction between Op18 and tubulin and that this tight binding requires the C-terminus of Op18; however, under conditions in which Op18 binds weakly to tubulin (pH 7.5), Op18 stimulated catastrophes without altering tubulin subunit association or dissociation rates, and Op18 did not depolymerize microtubules capped with guanylyl (α, β)-methylene diphosphonate–tubulin subunits. We hypothesize that weak binding between Op18 and tubulin results in free Op18, which is available to interact with microtubule ends and thereby promote catastrophes by a mechanism that likely involves GTP hydrolysis.