Normalization and Charter 77 : Violence, Commitment and Resistance in Czechoslovakia

In Czechoslovakia, the occupation of 1968 denoted the beginning of normalization , a political and societal stagnation that lasted two decades. Dissident initiative Charter 77 emerged in 1977, demanding that the leaders of the country respect human rights. The Helsinki process provided a macro-level framework that influenced opposition and dissident activities throughout Eastern Europe. The study contributes a focused empirical analysis of the period of normalization and the dissident movement Charter 77. Dissent in general is seen as an existential attitude; it can be encapsulated as a morally rationalized critical stance as derived from shared experience or interpretation of injustice, which serves as a basis for a shared collective identity comprising oppositional consciousness as one unifying factor. The study suggests that normalization can be understood as a fundamentally violent process and discusses the structural and cultural manifestations of violence with relation to Charter 77. In general, the aim of the system was to passivize the society to such an extent that it would not constitute a potential threat to the hegemonic rule of the regime. Normalization caused societal stagnation and apoliticization, but it also benefited those who accepted the new political reality. The study, however, questions the image of Czechoslovakia s allegedly highly repressive rule by showing that there was also quite considerable tolerance of Charter 77 and consideration before severe repression was brought to bear against dissidents. Furthermore, the study provides understanding of the motives and impetuses behind dissent, the strategic shifts in Charter 77 activities, and the changes in the regime s policies toward Charter 77. The study also adds new perspective on the common image of Charter 77 as a non political initiative and suggests that Charter 77 was, in fact, a political entity, an actively political one in the latter half of the 1980s. Charter 77 was a de facto hybrid of a traditional dissident initiative and an oppositional actor. Charter 77 adopted a two-dimension approach: firstly, it still emphasized its role as a citizens initiative supporting human rights, but, secondly, at the same time, it was a directly political actor supporting and furthering the development of political opposition against the ruling power.

Endoplasmic reticulum stress and cell death mechanisms in the cell model of Huntington’s disease

This thesis clarifies important molecular pathways that are activated during the cell death observed in Huntington’s disease. Huntington’s disease is one of the most common inherited neurodegenerative diseases, which is primarily inherited in an autosomal dominant manner. HD is caused by an expansion of CAG repeats in the first exon of the IT15 gene. IT15 encodes the production of a Huntington’s disease protein huntingtin. Mutation of the IT15 gene results in a long stretch of polyQ residues close to the amino-terminal region of huntingtin. Huntington’s disease is a fatal autosomal neurodegenerative disorder. Despite the current knowledge of HD, the precise mechanism behind the selective neuronal death, and how the disease propagates, still remains an enigma. The studies mainly focused on the control of endoplasmic reticulum (ER) stress triggered by the mutant huntingtin proteins. The ER is a delicate organelle having essential roles in protein folding and calcium regulation. Even the slightest perturbations on ER homeostasis are effective enough to trigger ER stress and its adaptation pathways, called unfolded protein response (UPR). UPR is essential for cellular homeostasis and it adapts ER to the changing environment and decreases ER stress. If adaptation processes fail and stress is excessive and prolonged; irreversible cell death pathways are engaged. The results showed that inhibition of ER stress with chemical agents are able to decrease cell death and formation of toxic cell aggregates caused by mutant huntingtin proteins. The study concentrated also to the NF-κB (nuclear factor-kappaB) pathway, which is activated during ER stress. NF-κB pathway is capable to regulate the levels of important cellular antioxidants. Cellular antioxidants provide a first line of defence against excess reactive oxygen species. Excess accumulation of reactive oxygen species and subsequent activation of oxidative stress damages motley of vital cellular processes and induce cell degeneration. Data showed that mutant huntingtin proteins downregulate the expression levels of NF-κB and vital antioxidants, which was followed by increased oxidative stress and cell death. Treatment with antioxidants and inhibition of oxidative stress were able to counteract these adverse effects. In addition, thesis connects ER stress caused by mutant huntingtin to the cytoprotective autophagy. Autophagy sustains cellular balance by degrading potentially toxic cell proteins and components observed in Huntington’s disease. The results revealed that cytoprotective autophagy is active at the early points (24h) of ER stress after expression of mutant huntingtin proteins. GADD34 (growth arrest and DNA damage-inducible gene 34), which is previously connected to the regulation of translation during cell stress, was shown to control the stimulation of autophagy. However, GADD34 and autophagy were downregulated at later time points (48h) during mutant huntingtin proteins induced ER stress, and subsequently cell survival decreased. Overexpression GADD34 enhanced autophagy and decreased cell death, indicating that GADD34 plays a critical role in cell protection. The thesis reveales new interesting data about the neuronal cell death pathways seen in Huntington’s disease, and how cell degeneration is partly counteracted by various therapeutic agents. Expression of mutant huntingtin proteins is shown to alter signaling events that control ER stress, oxidative stress and autophagy. Despite that Huntington’s disease is mainly an untreatable disorder; these findings offer potential targets and neuroprotective strategies in designing novel therapies for Huntington’s disease.

The death of newspapers: Have we reached the tipping point?

News Corp’s only substantial competitor in the print journalism sector may be on the brink of giving up the ghost, as has long been speculated even by its natural supporters such as Beecher. If it does, hundreds more jobs will go, along with the many hundreds of experienced, skilled journalists and editors already shown the door by the company.

Specific immunoneutralization of FSH leads to apoptotic cell death of the pachytene spermatocytes and spermatogonial cells in the rat

Although requirement for follicle stimulating hormone (FSH) in the initiation of spermatogenesis is well documented, its role in adult spermatogenesis is still debated. In the present communication, we have investigated the effect of specific immunoneutralization of FSH on apoptotic cell death in the testicular germ cells both in immature and adult rats. The germ cells of control animals showed predominantly high molecular weight DNA while the antiserum (a/s) treated group showed DNA fragmentation characteristic of apoptosis. The pattern could be detected within 24 hours of a/s treatment, and became more pronounced after 48 hours. The germ cells were purified from FSH a/s treated rats by centrifugal elutriation and vulnerability of each cell type to undergo apoptosis on FSH neutralization was investigated. The pachytene spermatocytes were found to be most sensitive to absence of FSH, even in the adult animals suggesting the involvement of FSH in spermatogenesis. The in situ analysis of DNA strand breakage following FSH a/s treatment showed fragmentation of the DNA of the pachytene spermatocytes confirming this observation. The in situ analysis also showed that the spermatogonia undergo apoptosis in addition to the pachytene spermatocytes. These data clearly demonstrate the role of FSH in the adult rat spermatogenesis.

Development of salinity tolerance in rice by constitutive-overexpression of genes involved in the regulation of programmed cell death

Environmental factors contribute to over 70% of crop yield losses worldwide. Of these drought and salinity are the most significant causes of crop yield reduction. Rice is an important staple crop that feeds more than half of the world’s population. However among the agronomically important cereals rice is the most sensitive to salinity. In the present study we show that exogenous expression of anti-apoptotic genes from diverse origins, AtBAG4 (Arabidopsis), Hsp70 (Citrus tristeza virus) and p35 (Baculovirus), significantly improves salinity tolerance in rice at the whole plant level. Physiological, biochemical and agronomical analyses of transgenic rice expressing each of the anti-apoptotic genes subjected to salinity treatment demonstrated traits associated with tolerant varieties including, improved photosynthesis, membrane integrity, ion and ROS maintenance systems, growth rate, and yield components. Moreover, FTIR analysis showed that the chemical composition of salinity-treated transgenic plants is reminiscent of non-treated, unstressed controls. In contrast, wild type and vector control plants displayed hallmark features of stress, including pectin degradation upon subjection to salinity treatment. Interestingly, despite their diverse origins, transgenic plants expressing the anti-apoptotic genes assessed in this study displayed similar physiological and biochemical characteristics during salinity treatment thus providing further evidence that cell death pathways are conserved across broad evolutionary kingdoms. Our results reveal that anti-apoptotic genes facilitate maintenance of metabolic activity at the whole plant level to create favorable conditions for cellular survival. It is these conditions that are crucial and conducive to the plants ability to tolerate/adapt to extreme environments.

Death pathways activated in the neurotrophic factor-deprived neurons

Programed cell death (PCD) is a fundamental biological process that is as essential for the development and tissue homeostasis as cell proliferation, differentiation and adaptation. The main mode of PCD - apoptosis - occurs via specifi c pathways, such as mitochondrial or death receptor pathway. In the developing nervous system, programed death broadly occurs, mainly triggered by the defi ciency of different survival-promoting neurotrophic factors, but the respective death pathways are poorly studied. In one of the best-characterized models, sympathetic neurons deprived of nerve growth factor (NGF) die via the classical mitochondrial apoptotic pathway. The main aim of this study was to describe the death programs activated in these and other neuronal populations by using neuronal cultures deprived of other neurotrophic factors. First, this study showed that the cultured sympathetic neurons deprived of glial cell line-derived neurotrophic factor (GDNF) die via a novel non-classical death pathway, in which mitochondria and death receptors are not involved. Indeed, cytochrome c was not released into the cytosol, Bax, caspase-9, and caspase-3 were not involved, and Bcl-xL overexpression did not prevent the death. This pathway involved activation of mixed lineage kinases and c-jun, and crucially requires caspase-2 and -7. Second, it was shown that deprivation of neurotrophin-3 (NT-3) from cultured sensory neurons of the dorsal root ganglia kills them via a dependence receptor pathway, including cleavage of the NT- 3 receptor TrkC and liberation of a pro-apoptotic dependence domain. Indeed, death of NT-3-deprived neurons was blocked by a dominant-negative construct interfering with TrkC cleavage. Also, the uncleavable mutant of TrkC, replacing the siRNA-silenced endogeneous TrkC, was not able to trigger death upon NT-3 removal. Such a pathway was not activated in another subpopulation of sensory neurons deprived of NGF. Third, it was shown that cultured midbrain dopaminergic neurons deprived of GDNF or brainderived neurotrophic factor (BDNF) kills them by still a different pathway, in which death receptors and caspases, but not mitochondria, are activated. Indeed, cytochrome c was not released into the cytosol, Bax was not activated, and Bcl-xL did not block the death, but caspases were necessary for the death of these neurons. Blocking the components of the death receptor pathway - caspase-8, FADD, or Fas - blocked the death, whereas activation of Fas accelerated it. The activity of Fas in the dopaminergic neurons could be controlled by the apoptosis inhibitory molecule FAIML. For these studies we developed a novel assay to study apoptosis in the transfected dopaminergic neurons. Thus, a novel death pathway, characteristic for the dopaminergic neurons was described. The study suggests death receptors as possible targets for the treatment of Parkinson s disease, which is caused by the degeneration of dopaminergic neurons.

Ballistic Trauma in Finland : An Epidemiologic and Clinical Study of Firearm and Explosion Injuries

The occurrence and nature of civilian firearm- and explosion-injuries in Finland, and the nature of severe gunshot injuries of the extremities were described in seven original articles. The main data sources used were the National Hospital Discharge Register, the Cause-of-Death Register, and the Archive of Death Certificates at Statistics Finland. The present study was population based. Epidemiologic methods were used in six and clinical analyses in five papers. In these clinical studies, every original hospital record and death certificate was critically analyzed. The trend of hospitalized firearm injuries has slightly declined in Finland from the late 1980s to the early 2000s. The occurrence decreased from 5.1 per 100 000 person-years in 1990 to 2.6 in 2003. The decline was found in the unintentional firearm injuries. A high incidence of unintentional injuries by firearms was characteristic of the country, while violence and homicides by firearms represented a minor problem. The incidence of fatal non-suicidal firearm injuries has been stable, 1.8 cases per 100 000 person-years. Suicides using firearms were eight times more common during the period studied. This is contrary to corresponding reports from many other countries. However, the use of alcohol and illegal drugs or substances was detected in as many as one-third of the injuries studied. The median length of hospitalization was three days and it was significantly associated (p<0.001) with the type of injury. The mean length of hospital stay has decreased from the 1980s to the early 2000s. In this study, there was a special interest in gunshot injuries of the extremities. From a clinical point of view, the nature of severe extremital gunshot wounds, as well as the primary operative approach in their management, varied. The patients with severe injuries of this kind were managed at university and central hospital emergency departments, by general surgeons in smaller hospitals and by cardiothoracic or vascular surgeons in larger hospitals. Injuries were rarities and as such challenges for surgeons on call. Some noteworthy aspects of the management were noticed and these should be focused on in the future. On the other hand, the small population density and the relatively large geographic area of Finland do not favor high volume, centralized trauma management systems. However, experimental war surgery has been increasingly taught in the country from the 1990s, and excellent results could be expected during the present decade. Epidemiologically, explosion injuries can be considered a minor problem in Finland at present, but their significance should not be underestimated. Fatal explosion injuries showed up sporadically. An increase occurred from 2002 to 2004 for no obvius reason. However, in view of the historical facts, a possibility for another rare major explosion involving several people might become likely within the next decade. The national control system of firearms is mainly based on the new legislations from 1998 and 2002. However, as shown in this study, there is no reason to assume that the national hospitalization policies, or the political climate, or the legislation might have changed over the study period and influenced the declining development, at least not directly. Indeed, the reason for the decline to appear in the incidence of unintentional injuries only remains unclear. It may derive from many practical steps, e.g. locked firearm cases, or from the stability of the community itself. For effective reduction of firearm-related injuries, preventive measures, such as education and counseling, should be targeted at recreational firearm users. To sum up, this study showed that the often reported increasing trend in firearm as well as explosion-related injuries has not manifested in Finland. Consequently, it can be recognized that, overall, the Finnish legislation together with the various strategies have succeeded in preventing firearm- and explosion-related injuries in the country.

Decision-making in a death investigation: Emotions, families and the coroner

The role of the coroner in common law countries such as Australia, England, Canada and New Zealand is to preside over death investigations where there is uncertainty as to the manner of death, a need to identify the deceased, a death of unknown cause, or a violent or unnatural death. The vast majority of these deaths are not suspicious and thus require coroners to engage with grieving families who have been thrust into a legal process through the misfortune of a loved one's sudden or unexpected death. In this research, 10 experienced coroners discussed how they negotiated the grief and trauma evident in a death investigation. In doing so, they articulated two distinct ways in which legal officers engaged with emotions, which are also evident in the literature. The first engages the script of judicial dispassion, articulating a hierarchical relationship between reason and emotion, while the second introduces an ethic of care via the principles of therapeutic jurisprudence, and thus offers a challenge to the role of emotion in the personae of the professional judicial officer. By using Hochschild's work on the sociology of emotions, this article discusses the various ways in which coroners manage the emotion of a death investigation through emotion work. While emotional distance may be an understandable response by coroners to the grief and trauma experienced by families and directed at cleaner coronial decision-making, the article concludes that coroners may be better served by offering emotions such as sympathy, consideration and compassion directly to the family in those situations where families are struggling to accept, or are resistant to, coroners' decisions.

Causes of death in patients with rheumatoid arthritis over a 40-year period : with special emphasis on autopsy

Rheumatoid arthritis (RA) patients have premature mortality. Contrary to the general population, mortality in RA has not declined over time. This study aimed to evaluate determinants of mortality in RA by examining causes of death (CoDs) over time, accuracy of CoD diagnoses, and contribution of RA medication to CoDs. This study further evaluated detection rate of reactive systemic amyloid A amyloidosis, which is an important contributor to RA mortality. CoDs were examined in 960 RA patients between 1971 and 1991 (Study population A) and in 369 RA patients autopsied from 1952 to 1991, with non-RA patients serving as the reference cases (Study population B). In Study population B, CoDs by the clinician before autopsy were compared to those by the pathologist at autopsy to study accuracy of CoD diagnoses. In Study population B, autopsy tissue samples were re-examined systematically for amyloidosis (90% of patients) and clinical data for RA patients was studied from 1973. RA patients died most frequently of cardiovascular diseases (CVDs), infections, and RA. RA deaths declined over time. Coronary deaths showed no major change in Study population A, but, in Study population B, coronary deaths in RA patients increased from 1952 to 1991, while non-RA cases had a decrease in coronary deaths starting in the 1970s. Between CoD diagnoses by the clinician and those by the pathologist, RA patients had lower agreement than non-RA cases regarding cardiovascular (Kappa reliability measure: 0.31 vs. 0.51) and coronary deaths (0.33 vs. 0.46). Use of disease modifying anti-rheumatic drugs was not associated with any CoD. In RA patients, re-examination of autopsy tissue samples doubled the prevalence of amyloid compared with the original autopsy: from 18% to 30%. In the amyloid-positive RA patients, amyloidosis was diagnosed before autopsy in only 37%; and they had higher inflammatory levels and longer duration of RA than amyloid-negative RA patients. Of the RA patients with amyloid, only half had renal failure or proteinuria during lifetime. In RA, most important determinants of mortality were CVDs, RA, and infections. In RA patients, RA deaths decreased over time, but this was not true for coronary deaths. Coronary death being less accurately diagnosed in RA may indicate that coronary heart disease (CHD) often goes unrecognized during lifetime. Thus, active search for CHD and its effective treatment is important to reduce cardiovascular mortality. Reactive amyloidosis may often go undetected. In RA patients with proteinuria or renal failure, as well as with active and long-lasting RA, a systematic search for amyloid is important to enable early diagnosis and early enhancement of therapy. This is essential to prevent clinical manifestations of amyloidosis such as renal failure, which has a poor prognosis.

Fighting like a girl … or a boy? An analysis of videos of violence between young girls posted on online fight websites

How young women engage in physical violence with other young women is an issue that raises specific concerns in both criminological literature and theories. Current theoretical explanations construct young women’s violence in one of two ways: young women are not physically violent at all, and adhere to an accepted performance of hegemonic femininity; or young women reject accepted performances of hegemonic femininity in favour of a masculine gendered performance to engage in violence successfully. This article draws on qualitative and quantitative data obtained from a structured observation and thematic analysis of 60 online videos featuring young women’s violent altercations. It argues that, contrary to this dichotomous construction, there appears to be a third way young women are performing violence, underpinned by masculine characteristics of aggression but upholding a hegemonic feminine gender performance. In making this argument, this article demonstrates that a more complex exploration and conceptualisation of young women’s violence, away from gendered constructs, is required for greater understanding of the issue.