Liberty

In terms of critical discourse, Liberty contributes to the ongoing aesthetic debate on ‘the sublime.’ Philosopher Immanuel Kant (1724–1804) defined the sublime as a failure of rationality in response to sensory overload: a state where the imagination is suspended, without definitive reference points—a state beyond unequivocal ‘knowing.’ I believe the events of September 11, 2001 eluded our understanding in much the same way, leaving us in a moment of suspension between awe and horror. It was an event that couldn’t be understood in terms of scope or scale. It was a moment of overload, which is so difficult to capture in art. With my work I attempt to rekindle that moment of suspension. Like the events of 9/11, Liberty defies definition. Its form is constantly changing; it is always presenting us with new layers of meaning. Nobody quite had a handle on the events that followed 9/11, because the implications were constantly shifting. In the same way, Liberty cannot be contained or defined at any moment in time. Like the events of 9/11, the full story cannot be told in a snapshot. One of the dictionary definitions for the word ‘sublime’ is the conversion of ‘a solid substance directly into a gas, without there being an intermediate liquid phase’. With this in mind, I would like to present Liberty as a work that is literally ‘sublime.’ But what’s really interesting to me about Liberty is that it presents the sublime on all levels: in its medium, in its subject matter (that moment of suspension), and in its formal (formless) presentation. On every level Liberty is sublime—subverting all tangible reference points and eluding capture entirely. Liberty is based on the Statue of Liberty in New York. However, unlike that statue which has stood in New York since 1886 and can be reasonably expected to stand for millennia, this work takes on diminishing proportions, carved as it is in carbon dioxide, a mysterious, previously unexplored medium—one which smokes, snows and dramatically vanishes into a harmless gas. Like the material this work is carved from, the civil liberties of the free world are diminishing fast, since 9/11 and before. This was my thought when I first conceived this work. Now it’s become evident that Liberty expresses a lot more than just this: it demonstrates the erosion of civil liberties, yes. However, it also presents the intangible, indefinable moments in the days and months that followed 9/11. The sculptural work will last for only a short time, and thereafter will exist only in documentation. During this time, the form is continually changing and self-refining, until it disappears entirely, to be inhaled, metabolised and literally taken to heart by viewers.

Liberty relighting, 20 years later

Recognized around the world as a powerful beacon for freedom, hope, and opportunity, the Statue of Liberty's light is not just metaphorical: her dramatic illumination is a perfect example of American ingenuity and engineering. Since the statue's installation in New York Harbor in 1886, lighting engineers and designers had struggled to illuminate the 150-foot copper-clad monument in a manner becoming an American icon. It took the thoughtful and creative approach of Howard Brandston-a legend in his own right-to solve this lighting challenge. In 1984, the designer was asked to give the statue a much-needed lighting makeover in preparation for its centennial. In order to avoid the shortcomings of previous attempts, he studied the monument from every angle and in all lighting conditions, discovering that it looked best in the light of dawn. Brandston determined that he would need 'one lamp to mimic the morning sun and one lamp to mimic the morning sky.' Learning that no existing lamps could simulate these conditions, Brandston partnered with General Electric to develop two new metal halide products. With only a short time for R&D, a team of engineers at GE's Nela Park laboratories assembled a 'top secret' testing room dedicated to the Statue of Liberty project. After nearly two years of work to perfect the new lamps, the 'dawn's early light' effect was finally achieved just days before the centennial celebrations were to take place in 1986. 'It was truly a labor of love,' he recalls.

Deprivation is an independent predictor of 1-year mortality in outpatients with chronic obstructive pulmonary disease

Deprivation is linked to increased incidence in a number of chronic diseases but its relationship to chronic obstructive pulmonary disease (COPD) is uncertain despite suggestions that the socioeconomic gradient seen in COPD is as great, if not greater, than any other disease (Prescott and Vestbo).1 There is also a need to take into account the confounding effects of malnutrition which have been shown to be independently linked to increased mortality (Collins et al).2 The current study investigated the influence of social deprivation on 1-year survival rates in COPD outpatients, independently of malnutrition. 424 outpatients with COPD were routinely screened for malnutrition risk using the ‘Malnutrition Universal Screening Tool’; ‘MUST’ (Elia),3 between July and May 2009; 222 males and 202 females; mean age 73 (SD 9.9) years; body mass index 25.8 (SD 6.3) kg/m2. Each individual's deprivation was calculated using the index of multiple deprivation (IMD) which was established according to the geographical location of each patient's address (postcode). IMD includes a number of indicators covering economic, housing and social issues (eg, health, education and employment) into a single deprivation score (Nobel et al).4 The lower the IMD score, the lower an individual's deprivation. The IMD was assigned to each outpatient at the time of screening and related to1-year mortality from the date screened. Outpatients who died within 1-year of screening were significantly more likely to reside within a deprived postcode (IMD 19.7±SD 13.1 vs 15.4±SD 10.7; p=0.023, OR 1.03, 95% CI 1.00 to 1.06) than those that did not die. Deprivation remained a significant independent risk factor for 1-year mortality even when adjusted for malnutrition as well as age, gender and disease severity (binary logistic regression; p=0.008, OR 1.04, 95% CI 1.04 to 1.07). Deprivation was not associated with disease-severity (p=0.906) or body mass index, kg/m2 (p=0.921) using ANOVA. This is the first study to show that deprivation, assessed using IMD, is associated with increased 1-year mortality in outpatients with COPD independently of malnutrition, age and disease severity. Deprivation should be considered in the targeted management of these patients.

The influence of deprivation domains on malnutrition risk in outpatients with chronic obstructive pulmonary disease

Deprivation assessed using the Index of Multiple Deprivation (IMD) has been shown to be an independent risk factor for both malnutrition and mortality in outpatients with chronic obstructive pulmonary disease (COPD) (Collins et al., 2010a, b). IMD consists of a range of different deprivation domains, although it is unclear which ones are most closely linked to malnutrition. The aim of the current study was to investigate whether the relationship between malnutrition and deprivation was a general one, affecting all domains in a consistent manner, or specific, affecting only certain domains.

The effect of overnight sleep deprivation after competitive rugby league matches on postmatch physiological and perceptual recovery

PURPOSE: This study examined the effects of overnight sleep deprivation on recovery following competitive rugby league matches. METHODS: Eleven male, amateur rugby league players performed two competitive matches, followed by either a normal night's sleep (~8h; CONT) or a sleep deprived night (~0h; SDEP) in a randomised fashion. Testing was conducted the morning of the match, and immediately post-match, 2h post and the next morning (16h post-match). Measures included counter-movement jump (CMJ) distance, knee extensor maximal voluntary contraction (MVC), voluntary activation (VA), venous blood creatine kinase (CK) and C-reactive protein (CRP), perceived muscle soreness and a word-colour recognition cognitive function test. Percent change between post- and 16h post-match was reported to determine the effect of the intervention the next morning. RESULTS: Large effects indicated a greater post- to 16h post-match percentage decline in CMJ distance following SDEP compared to CONT (P=0.10-0.16; d=0.95-1.05). Similarly, the percentage decline in incongruent word-colour reaction times were increased in SDEP trials (P=0.007; d=1.75). Measures of MVC did not differ between conditions (P=0.40-0.75; d=0.13-0.33), though trends for larger percentage decline in VA were detected in SDEP (P=0.19; d=0.84). Further, large effects indicated higher CK and CRP responses 16h post-match during SDEP compared to CONT (P=0.11-0.87; d=0.80-0.88). CONCLUSIONS: Sleep deprivation negatively affected recovery following a rugby league match, specifically impairing CMJ distance and cognitive function. Practitioners should promote adequate post-match sleep patterns or adjust training demands the next day to accommodate the altered physical and cognitive state following sleep deprivation.

The effects and interactions of GABAergic and dopaminergic agents in the prevention of form deprivation myopia by brief periods of normal vision

Intravitreal injections of GABA antagonists, dopamine agonists and brief periods of normal vision have been shown separately to inhibit form-deprivation myopia (FDM). Our study had three aims: (i) establish whether GABAergic agents modify the myopia protective effect of normal vision, (ii) investigate the receptor sub-type specificity of any observed effect, and (iii) consider an interaction with the dopamine (DA) system. Prior to the period of normal vision GABAergic agents were applied either (i) individually, (ii) in combination with other GABAergic agents (an agonist with an antagonist), or (iii) in combination with DA agonists and antagonists. Water injections were given to groups not receiving drug treatments so that all experimental eyes received intravitreal injections. As shown previously, constant form-deprivation resulted in high myopia and when diffusers were removed for 2 h per day the period of normal vision greatly reduced the FDM that developed. GABA agonists inhibited the protective effect of normal vision whereas antagonists had the opposite effect. GABAA/C agonists and D2 DA antagonists when used in combination were additive in suppressing the protective effect of normal vision. A D2 DA agonist restored some of the protective effect of normal vision that was inhibited by a GABA agonist (muscimol). The protective effect of normal vision against form-deprivation is modifiable by both the GABAergic and DAergic pathways.

Escape from apoptosis after prolonged serum deprivation is associated with the regulation of the mitochondrial death pathway by Bcl-x(l)

Bcl-x(l) and Bax play important roles in the regulation of apoptosis. This study investigated the involvement of the mitochondrial death pathway and the role of Bcl-x(l) and Bax in the escape from apoptosis after prolonged serum deprivation in Madin-Darby canine kidney (MDCK) cells. Low level apoptosis and basal activity of the mitochondrial death pathway were detectable in normal cell growth. In serum deprivation, mitosis was partially suppressed, and the mitochondrial activity was stimulated. The level of apoptosis continuously rose over 48 h. This rise was concomitant with the increasing presence of cytochrome c in cytosol. However, both apoptosis and cytosolic cytochrome c fell dramatically at 72 h. Elevation of whole cell Bcl-x(l) and redistribution of Bcl-x(l) protein from cytosol to the membrane at 48 h and 72 h was observed. Redistribution of Bax protein from the membrane to cytosol occurred at 24 h, and remained steady to 72 h. Bax/Bcl-x(l) coimmunoprecipitation by anti-Bax antibody showed reduced Bax/Bcl-x(l) interaction at the membrane at 72 h, but not at 24 or 48 h. These results suggest that apoptosis upon serum withdrawal results from the leakage of cytochrome c to cytosol. Amelioration of the leakage of cytochrome c and apoptosis requires not only the increase of Bcl-x(l)/Bax ratio, but also the release of Bcl-x(l) from Bax at the membrane.

The effect of sleep deprivation on BOLD activity elicited by a divided attention task

Sleep loss, widespread in today’s society and associated with a number of clinical conditions, has a detrimental effect on a variety of cognitive domains including attention. This study examined the sequelae of sleep deprivation upon BOLD fMRI activation during divided attention. Twelve healthy males completed two randomized sessions; one after 27 h of sleep deprivation and one after a normal night of sleep. During each session, BOLD fMRI was measured while subjects completed a cross-modal divided attention task (visual and auditory). After normal sleep, increased BOLD activation was observed bilaterally in the superior frontal gyrus and the inferior parietal lobe during divided attention performance. Subjects reported feeling significantly more sleepy in the sleep deprivation session, and there was a trend towards poorer divided attention task performance. Sleep deprivation led to a down regulation of activation in the left superior frontal gyrus, possibly reflecting an attenuation of top-down control mechanisms on the attentional system. These findings have implications for understanding the neural correlates of divided attention and the neurofunctional changes that occur in individuals who are sleep deprived.

Inhibition of form-deprivation myopia by a GABAAOr receptor antagonist, (1,2,5,6-tetrahydropyridin-4-yl) methylphosphinic acid (TPMPA), in guinea pigs

Purpose To investigate the effects of the relatively selective GABAAOr receptor antagonist (1,2,5,6-tetrahydropyridin-4-yl) methylphosphinic acid (TPMPA) on form-deprivation myopia (FDM) in guinea pigs. Methods A diffuser was applied monocularly to 30 guinea pigs from day 10 to 21. The animals were randomized to one of five treatment groups. The deprived eye received daily sub-conjunctival injections of 100 μl TPMPA at a concentration of (i) 0.03 %, ( ii) 0.3 %, or (iii) 1 %, a fourth group (iv) received saline injections, and another (v) no injections. The fellow eye was left untreated. An additional group received no treatment to either eye. Prior to and at the end of the treatment period, refraction and ocular biometry were performed. Results Visual deprivation produced relative myopia in all groups (treated versus untreated eyes, P < 0.05). The amount of myopia was significantly affected by the drug treatment (one-way ANOVA, P < 0.0001); myopia was less in deprived eyes receiving either 0.3 % or 1 % TPMPA (saline = −4.38 ± 0.57D, 0.3 % TPMPA = −3.00 ± 0.48D, P < 0.01; 1 % TPMPA = −0.88 ± 0.51D, P < 0.001). The degree of axial elongation was correspondingly less (saline = 0.13 ± 0.02 mm, 0.3 % TPMPA = 0.09 ± 0.01 mm, P < 0.01, 1 % TPMPA = 0.02 ± 0.01 mm, P < 0.001) as was the VC elongation (saline = 0.08 ± 0.01 mm, 0.3 % TPMPA = 0.05 ± 0.01 mm, P < 0.01, 1 % TPMPA = 0.01 ± 0.01 mm; P < 0.001). ACD and LT were not affected (one-way ANOVA, P > 0.05). One percent TPMPA was more effective at inhibiting myopia than 0.3 % (P < 0.01), and 0.03 % did not appreciably inhibit the myopia (0.03 % TPMPA versus saline, P > 0.05). Conclusions Sub-conjunctival injections of TPMPA inhibit FDM in guinea pig models in a dose-dependent manner.

The effect of deprivation and disease-severity on malnutrition risk in chronic obstructive pulmonary disease (COPD)

Deprivation has previously been shown to be an independent risk factor for the high prevalence of malnutrition observed in COPD (Collins et al., 2010). It has been suggested the socioeconomic gradient observed in COPD is greater than any other chronic disease (Prescott & Vestbo, 1999). The current study aimed to examine the infl uence of disease severity and social deprivation on malnutrition risk in outpatients with COPD. 424 COPD outpatients were screened using the ‘Malnutrition Universal Screening Tool’ (‘MUST’). COPD disease severity was recorded in accordance with the GOLD criteria and deprivation was established according to the patient’s geographical location (postcode) at the time of nutritional screening using the UK Government’s Index of Multiple Deprivation (IMD). IMD ranks postcodes from 1 (most deprived) to 32,482 (least deprived). Disease severity was posi tively associated with an increased prevalence of malnutrition risk (p < 0.001) both within and between groups, whilst rank IMD was negatively associated with malnutrition (p = 0.020), i.e. those residing in less deprived areas were less likely to be malnourished. Within each category of disease severity the prevalence of malnutrition was two-fold greater in those residing in the most deprived areas compared to those residing in the least deprived areas. This study suggests that deprivation and disease severity are independent risk factors for malnutrition in COPD both contributing to the widely variable prevalence of malnutrition. Consideration of these issues could assist with the targeted nutritional management of these patients.

Early maternal deprivation reduces prepulse inhibition and impairs spatial learning ability in adulthood: No further effect of post-pubertal chronic corticosterone treatment

Prolonged maternal deprivation leads to long-term alterations in hypothalamic–pituitary–adrenal (HPA) axis activity, disturbances of auditory information processing and neurochemical changes in the adult brain, some of which are similar to that observed in schizophrenia. Here we report the adult behavioural effects of maternal deprivation (12 h on postnatal days 9 and 11) in Wistar rats on paradigms of auditory information processing (prepulse inhibition), sensitivity to dopamimetics (amphetamine-induced hyper-locomotion) and cognition (T-maze delayed alternation and Morris water-maze). In addition, we examined the long-lasting effect of chronic 21-day corticosterone treatment during the post-pubertal period (i.e., postnatal days 56–76) on each of these behavioural paradigms in maternally deprived and control rats. Behavioural testing commenced 2 weeks after the termination of corticosterone treatment. Maternal deprivation led to a significant reduction in PPI and impaired spatial learning ability in adulthood, but did not affect the behavioural response to amphetamine. Post-pubertal chronic corticosterone treatment did not have any major long-lasting effects on any of the behavioural measures in either maternally deprived or control rats. Our findings further support maternal deprivation as an animal model of specific aspects of schizophrenia.

Adverse effects of androgen-deprivation therapy in prostate cancer and their management

Objective To provide an up-to-date summary of current literature on the management of adverse effects of androgen-deprivation therapy (ADT). Patients and Methods All relevant medical literature on men with prostate cancer treated with ADT from 2005 to 2014, and older relevant papers, were reviewed. Recent health advisory statements from the Australian government, societies and advocacy groups have been incorporated to the document. Results There are numerous adverse effects of ADT that require pro-active prevention and treatment. Ranging from cardiovascular disease, diabetes and osteoporosis, to depression, cognitive decline and sexual dysfunction, the range of adverse effects is wide. Baseline assessment, monitoring, prevention and consultation from a multidisciplinary team are important in minimising the harm from ADT. Conclusions This review provides a series of practical recommendations to assist with managing the adverse effects of ADT.

Dietary and exercise interventions to improve quality of life, metabolic risk factors and androgen deficiency symptoms in men with prostate cancer undergoing androgen deprivation therapy

Introduction Lifestyle interventions might be useful in the management of adverse effects of androgen deprivation therapy (ADT) in men with prostate cancer. Objectives To examine the effects of dietary and exercise interventions on quality of life (QoL), metabolic risk factors and androgen deficiency symptoms in men with prostate cancer undergoing ADT. Methods CINAHL, Cochrane library, Medline and PsychINFO were searched to identify randomised controlled trials published from January, 2004 to October, 2014. Data extraction and methodological quality assessment was independently conducted by two reviewers. Meta-analysis was conducted using RevMan® 5.3.5. Results Of 2183 articles retrieved, 11 studies met the inclusion criteria and had low risk of bias.Nine studies evaluated exercise (resistance and/or aerobic and/or counselling) and three evaluated dietary supplementation. Median sample size =79 (33–121) and median intervention duration was 12 weeks (12–24). Exercise improved QoL measures (SMD 0.26, 95%CI −0.01 to 0.53) but not body composition, metabolic risk or vasomotor symptoms. Qualitative analysis indicated soy (or isoflavone) supplementation did not improve vasomotor symptoms; however, may improve QoL. Conclusions Few studies have evaluated the efficacy of lifestyle interventions in the management of adverse effects of ADT. We found inconclusive results for exercise in improving QoL and negative results for other outcomes. For soy-based products, we found negative results for modifying vasomotor symptoms and inconclusive results for improving QoL. Future work should investigate the best mode of exercise for improving QoL and other interventions such as dietary counselling should be investigated for their potential to modify these outcomes.