Comparison of findings identified at traditional invasive autopsy and postmortem computed tomography in suicidal hangings.

Cases of suicidal hanging are a common death referred for medico-legal autopsy throughout the world. Although some advocate using postmortem computed tomography (PMCT) without traditional invasive autopsy (TIA) to investigate such deaths, others reject this approach. There is currently limited evidence to guide practice. In this context, the TIA reports and PMCT images of 50 cases of suspected suicidal hanging during an 11-month period were reviewed. The reviewers were blinded to the findings of the other modality. A Cohen's Kappa coefficient (K) was calculated to assess agreement between TIA and PMCT across a range of pertinent findings. This analysis demonstrated perfect agreement for identification of a ligature (K = 1.00) and a strong level of agreement for identification of a ligature suspension point (K = 0.832) but only a minimal level of agreement for overall ligature mark (K = 0.223). PMCT demonstrated a weak level of agreement for fractures of hyoid bone (K = 0.555) and thyroid cartilage (K = 0.538). Three probable fractures not identified at TIA were identified on PMCT. TIA was shown to be superior in the identification of intramuscular and laryngeal fracture-related haemorrhage/bruising whereas PMCT was superior to TIA in identifying body gas deposition. There was overall good correlation between the natural disease and trauma identified elsewhere in the body during the TIA and PMCT. The study demonstrates that PMCT can assist the investigation of suspected suicidal hangings. However, the accuracy of many findings is limited, and if it is used as an alternative to the TIA, potentially pertinent findings, such as fractures of the laryngeal cartilages, could be missed.

Clustered Kv2.1 decreases dopamine transporter activity and internalization.

The dopamine transporter (DAT) regulates dopamine neurotransmission via reuptake of dopamine released into the extracellular space. Interactions with partner proteins alter DAT function and thereby dynamically shape dopaminergic tone important for normal brain function. However, the extent and nature of these interactions are incompletely understood. Here, we describe a novel physical and functional interaction between DAT and the voltage-gated K+ channel Kv2.1 (potassium voltage-gated channel subfamily B member 1 or KCNB1). To examine the functional consequences of this interaction, we employed a combination of immunohistochemistry, immunofluorescence live-cell microscopy, co-immunoprecipitation, and electrophysiological approaches. Consistent with previous reports, we found Kv2.1 is trafficked to membrane-bound clusters observed both in vivo and in vitro in rodent dopamine neurons. Our data provide evidence that clustered Kv2.1 channels decrease DAT's lateral mobility and inhibit its internalization, while also decreasing canonical transporter activity by altering DAT's conformational equilibrium. These results suggest that Kv2.1 clusters exert a spatially discrete homeostatic braking mechanism on DAT by inducing a relative increase in inward-facing transporters. Given recent reports of Kv2.1 dysregulation in neurological disorders, it is possible that alterations in the functional interaction between DAT and Kv2.1 affect dopamine neuron activity.

Microglia and Other Myeloid Cells in Central Nervous System Health and Disease.

Mononuclear macrophages derived from the bone marrow (myeloid cells) are key cellular components of the innate immune system in different organs. In this minireview, we are focused on both brain and blood macrophages, known as microglia and monocytes, respectively. We provide a succinct summary of the cells' functions under both normal and pathologic conditions, with particular reference to common neurodegenerative disorders, such as Alzheimer and Parkinson disease. SIGNIFICANCE STATEMENT: In this minireview, we aim to summarize available literature on microglial and myeloid involvement in CNS disease, directing the reader toward relevant and translatable interpretations of myeloid cell function in CNS health and neurodegeneration.

Oesophagostomiasis in non-human primates of Gombe National Park, Tanzania.

Oesophagostomum sp. is a parasitic nematode that frequently infects wild chimpanzees. Although nodular lesions are commonly associated with infection, some wild chimpanzee populations seem to tolerate Oesophagostomum nodular lesions while those at Gombe and other sites suffer from associated morbidity and mortality. From August 2004 to December 2013, we examined demographic (i.e., age, sex) and individual correlates (i.e., fecal consistency, Oesophagostomum egg production) to Oesophagostomum-associated pathology in 14 individually recognized chimpanzees at Gombe Stream National Park, Tanzania. In addition, we characterized Oesophagostomum-associated pathology in 14 individual sympatric primates including baboons, colobus, and cercopithecid monkeys. In five chimpanzees, there was no evidence of any significant underlying disease aside from oesophagostomiasis to explain the thin condition or diarrhea. All five of these chimpanzees had moderate to numerous parasitic nodules. In general, nodules were more numerous in older chimpanzees. Three of four chimpanzees with the highest average Oesophagostomum egg counts in feces collected during the year prior to their death had numerous parasitic nodules at necropsy. In contrast, the four chimpanzees with the lowest egg counts had only moderate numbers of nodules. No association (P = 0.74) was noted between frequency of diarrhea in the year prior to death and the number of nodules noted at necropsy. Nodules were also present in all baboons examined documenting pathology associated with Oesophagostomum infection in wild baboons. In contrast, no lesions were noted in colobus or cercopithecid monkeys, although it is uncertain if they are infected as no fecal studies have been completed in these species to date at Gombe. Sequence of DNA isolated from nodules in chimpanzees matched (99%) Oesophagostomum stephanostomum. Further research is needed to identify the types of Oesophagostomum causing lesions in baboons and to determine if baboons suffer from these infections. Am. J. Primatol. 80:e22572, 2018. © 2016 Wiley Periodicals, Inc.

"Catch-and-release" of HNO with pyrazolones.

A new and versatile class of HNO donors, the (hydroxylamino)pyrazolone (HAPY) series of HNO donors utilizing pyrazolone (PY) leaving groups, is described. HNO, the smallest N-based aldehyde equivalent, is used as a reagent along with a variety of PY compounds to synthesize the desired HAPY donors in what can be considered an N-selective HNO-aldol reaction in up to quantitative yields. The bimolecular rate constant of HNO with PY in pH 7.4 phosphate buffer at 37 °C can reach 8 × 10(5) M(-1) s(-1). In (1)H NMR experiments, the HAPY compounds generate HNO quantitatively (trapped as a phosphine aza-ylide) with half-lives spanning 3 orders of magnitude (minutes to days) under physiologically relevant conditions. B3LYP/6-31G* calculations confirm the energetically favorable reactions between HNO and the PY enol and enolate, whereas HNO release is expected to occur through the oxyanion (OHN-PY) of each HAPY compound. HNO has been shown to provide functional support to failing hearts.

Inner Peace: Evaluating a Complementary Program Promoting Intra-Personal Peace at Adelaide Women's Prison, Australia.

The Peace Education Program, created in 2012, is a complementary program with potential to supplement official rehabilitation interventions offered in correctional centers. The program promotes "inner peace" as an innate and universal human resource, but whilst inner peace is a key concept in positive psychology and the Good Lives Model, there is a paucity of research regarding how to operationalize and evaluate this concept. The program had not previously been the subject of independent theoretically-informed research. Drawing on a mixed methods study conducted in Adelaide Women's Prison, this article explores the impact of the program on participants' learning regarding inner peace. Participants reported a greater understanding about inner peace, which they described as contributing to a stronger sense of their identity, enhanced self-esteem and increased self-regulation skills, resulting in reductions in impulsivity and reactive aggression. The quantitative data indicated there was a significant increase in participants' subjective ratings of inner peace before the program (M = 12.08) and post-program completion (M = 14.00) (p < .001). Growth in affect-regulation and anger-management skills may contribute to reductions in offending.

Altered stress stimulation of inward rectifier potassium channels in Andersen-Tawil syndrome.

Inward rectifier potassium channels of the Kir2 subfamily are important determinants of the electrical activity of brain and muscle cells. Genetic mutations in Kir2.1 associate with Andersen-Tawil syndrome (ATS), a familial disorder leading to stress-triggered periodic paralysis and ventricular arrhythmia. To identify the molecular mechanisms of this stress trigger, we analyze Kir channel function and localization electrophysiologically and by time-resolved confocal microscopy. Furthermore, we employ a mathematical model of muscular membrane potential. We identify a novel corticoid signaling pathway that, when activated by glucocorticoids, leads to enrichment of Kir2 channels in the plasma membranes of mammalian cell lines and isolated cardiac and skeletal muscle cells. We further demonstrate that activation of this pathway can either partly restore (40% of cases) or further impair (20% of cases) the function of mutant ATS channels, depending on the particular Kir2.1 mutation. This means that glucocorticoid treatment might either alleviate or deteriorate symptoms of ATS depending on the patient's individual Kir2.1 genotype. Thus, our findings provide a possible explanation for the contradictory effects of glucocorticoid treatment on symptoms in patients with ATS and may open new pathways for the design of personalized medicines in ATS therapy.

A novel dual-fluorescence strategy for functionally validating microRNA targets in 3' untranslated regions: regulation of the inward rectifier potassium channel K(ir)2.1 by miR-212.

Gene targeting by microRNAs is important in health and disease. We developed a functional assay for identifying microRNA targets and applied it to the K(+) channel K(ir)2.1 [KCNJ2 (potassium inwardly-rectifying channel, subfamily J, member 2)] which is dysregulated in cardiac and vascular disorders. The 3'UTR (untranslated region) was inserted downstream of the mCherry red fluorescent protein coding sequence in a mammalian expression plasmid. MicroRNA sequences were inserted into the pSM30 expression vector which provides enhanced green fluorescent protein as an indicator of microRNA expression. HEK (human embryonic kidney)-293 cells were co-transfected with the mCherry-3'UTR plasmid and a pSM30-based plasmid with a microRNA insert. The principle of the assay is that functional targeting of the 3'UTR by the microRNA results in a decrease in the red/green fluorescence intensity ratio as determined by automated image analysis. The method was validated with miR-1, a known down-regulator of K(ir)2.1 expression, and was used to investigate the targeting of the K(ir)2.1 3'UTR by miR-212. The red/green ratio was lower in miR-212-expressing cells compared with the non-targeting controls, an effect that was attenuated by mutating the predicted target site. miR-212 also reduced inward rectifier current and K(ir)2.1 protein in HeLa cells. This novel assay has several advantages over traditional luciferase-based assays including larger sample size, amenability to time course studies and adaptability to high-throughput screening.

An intervention to manage compassion fatigue in oncology nurses in Durban, South Africa.

Background: Oncology nurses are involved through the often protracted and potentially traumatic continuum of diagnosis and treatment of their patients, which places them at high risk of developing compassion fatigue. Aim: The aim of the study was to develop and implement an in-facility intervention to manage compassion fatigue among oncology nurses in Durban, South Africa. Setting: The study was conducted with oncology nurses at state, private (private health insurance) and non-governmental oncology facilities (Hospice). Methods: The Self-Care Intervention for Oncology Nurses was developed and implemented using action research with a mixed methods sequential explanatory design. It involved an integrative review, Professional Quality of Life (ProQOL) v 5 questionnaires (n = 83) and in-depth individual interviews (n = 8). Results: Developed from the findings of the integrative review, quantitative and qualitative data, the Self-Care Intervention for Oncology Nurses comprised three components, namely psycho-education on risks (booklet), practices of remembrance (remembrance tree) and support structures (support group and follow-up family call). Overall, the participants enjoyed reading the booklet and engaging in the support group. There were varied responses to the remembrance tree and hesitancy to partaking in the follow-up phone call. Conclusion: The developed intervention could encourage awareness of compassion fatigue amongst oncology nurses' engagement in self-care practices such as symbolic remembrance of patients and recognition of the value of support structures. Contribution: The intervention may assist oncology nurses in the provision of compassionate caring for their patients and potentially minimise compassion fatigue.

Awareness of inappropriate use related to antimicrobial resistance among medical doctors by country economic status: A systematic review.

BACKGROUND: Antimicrobial resistance (AMR) is promoted by inappropriate use and is a greater burden for low to middle income countries (LMIC) than high income countries (HIC). OBJECTIVE: This systematic review aimed to compare the awareness of inappropriate use related to AMR among medical doctors from LMIC and HIC using published knowledge, attitude and practice (KAP) studies. METHODS: Following Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines, sequential systematic literature search of PubMed and Web of Science databases for articles published since inception up to June 1, 2022 for KAP studies involving medical doctors. Using fifteen KAP items related to promoting AMR, data on proportion of participants responding affirmatively was extracted and reported using means, ranges and 95% confidence intervals (CI). RESULTS: Forty-two studies met the inclusion criteria and involved 13,089 medical doctors from 11HIC and 21LMIC. All were cross-sectional studies, 71.4% involved non-probability sampling and 78.6% were of satisfactory quality. Knowledge items showed mean proportion of more medical doctors responding correctly. Similar affirmation trends were observed for attitude and prescribing practice items. Awareness appeared similar between medical doctors of the economic groups, except for a greater interest in training for LMIC (95.4%; 95%CI 93.0%, 97.9%) versus HIC (81.7%; 95%CI 65.6%, 97.9%). Countries with poor proportions were identified in both economic groups. CONCLUSION: For identified studies, trends suggest good awareness among medical doctors of the known inappropriate use and perceived threat of AMR, as well as prescribing practices to reduce the risk of AMR. Trends were similar across HIC and LMIC; however, countries with evidence of poor awareness exist in both economic groups.

Pathologic lesions in chimpanzees (Pan trogylodytes schweinfurthii) from Gombe National Park, Tanzania, 2004-2010.

During a population decline or disease outbreak, the true risk of specific diseases to a wild population is often difficult to determine because of a lack of baseline disease information. To better understand the risk of disease in an endangered and scientifically important population of chimpanzees (Pan trogylodytes schweinfurthii), a health monitoring program was initiated in Gombe National Park, Tanzania. As part of this health monitoring program, comprehensive necropsies with histopathology were conducted on chimpanzees (n = 11; 5 male, 6 female), ranging in age from fetal to 44 yr, that were found dead between August 2004 and January 2010. In contrast to previous reports, respiratory disease was not noted as a cause of morbidity or mortality. Trauma was the most common cause of death in these 11 chimpanzees. All of the chimpanzees greater than 1 yr of age had intestinal and mesenteric parasitic granulomas associated with true strongyles consistent with Oesophagostomum spp. The relative numbers of granulomas increased with age and, in some cases, may have been a cause of weight loss and diarrhea. Simian immunodeficiency virus (SIV)cpz infection was documented in four deceased apes, all of whom exhibited varying amounts of lymphoid depletion including two females with marked CD4+ T cell loss consistent with endstage SIVmac or human immunodeficiency virus infections. Myocardial megalokaryosis was common in chimpanzees greater than 1 mo of age; yet myocardial interstitial fibrosis, a common lesion in captive chimpanzees, was uncommon and only noted in two aged chimpanzees. These findings provide important information on causes of morbidity and mortality in wild chimpanzees, information that can be used to interpret findings during population declines and lead to better management of this population in the context of disease risk.

'I've become so healthy that I can't live anymore': exploring 'health as balance' discourses and the construction of health and identity among young urban South African adults.

Social science research on health in South Africa tends to focus on illness and how to address health problems. Qualitative empirical research focussing on lay understandings and experiences of healthiness, or health discourses, in South Africa is fairly limited. This article addresses this gap by critically exploring how young South African adults used discourses of balance to make sense of what it means to be a healthy person and highlights the implications of these discourses for identity. Foucault's concepts of 'technologies of the self' and 'techniques of discipline' are discussed as a theoretical grounding for this paper. Data were collected from 20 in-depth semi-structured interviews, and analysed using Foucauldian discourse analysis. This paper will specifically explore a key discourse identified through the analysis: 'health as balance' and 2 interrelated sub-discourses which fall within it. Through this discourse, healthiness was constructed as requiring a broad focus on improving all aspects of one's life ('health as holistic') and the avoidance of any behaviours or emotions which could be classified as extreme ('health as moderation'). Constant, careful management of the self, or 'calibration', functions to both perpetuate a cycle of 'anxiety and control' and to obscure ways in which health discourses can be harmful or problematic.

Antimicrobial Resistance Creates Threat to Chimpanzee Health and Conservation in the Wild.

Infectious disease is recognized as the greatest threat to the endangered chimpanzees made famous by the groundbreaking work of Dr. Jane Goodall at Gombe National Park (GNP), Tanzania. The permeable boundary of this small protected area allows for regular wildlife-human and wildlife-domestic animal overlap, which may facilitate cross-species transmission of pathogens and antimicrobial resistance. Few studies have examined the prevalence of antimicrobial resistance in wild ape populations. We used molecular techniques to investigate the presence of genes conferring resistance to sulfonamides (often used to treat diarrheal illness in human settings in this region) and tetracycline (used in the past-though much less so now) in fecal specimens from humans, domestic animals, chimpanzees, and baboons in and around GNP. We also tested stream water used by these groups. Sulfonamide resistance was common in humans (74%), non-human primates (43%), and domestic animals (17%). Tetracycline resistance was less common in all groups: humans (14%), non-human primates (3%), and domestic animals (6%). Sul resistance genes were detected from 4/22 (18%) of streams sampled. Differences in sul gene frequencies did not vary by location in humans nor in chimpanzees.

TNFα increases tyrosine hydroxylase expression in human monocytes.

Most, if not all, peripheral immune cells in humans and animals express tyrosine hydroxylase (TH), the rate limiting enzyme in catecholamine synthesis. Since TH is typically studied in the context of brain catecholamine signaling, little is known about changes in TH production and function in peripheral immune cells. This knowledge gap is due, in part, to the lack of an adequately sensitive assay to measure TH in immune cells expressing lower TH levels compared to other TH expressing cells. Here, we report the development of a highly sensitive and reproducible Bio-ELISA to quantify picogram levels of TH in multiple model systems. We have applied this assay to monocytes isolated from blood of persons with Parkinson's disease (PD) and to age-matched, healthy controls. Our study unexpectedly revealed that PD patients' monocytes express significantly higher levels of TH protein in peripheral monocytes relative to healthy controls. Tumor necrosis factor (TNFα), a pro-inflammatory cytokine, has also been shown to be increased in the brains and peripheral circulation in human PD, as well as in animal models of PD. Therefore, we investigated a possible connection between higher levels of TH protein and the known increase in circulating TNFα in PD. Monocytes isolated from healthy donors were treated with TNFα or with TNFα in the presence of an inhibitor. Tissue plasminogen activator (TPA) was used as a positive control. We observed that TNFα stimulation increased both the number of TH+ monocytes and the quantity of TH per monocyte, without increasing the total numbers of monocytes. These results revealed that TNFα could potentially modify monocytic TH production and serve a regulatory role in peripheral immune function. The development and application of a highly sensitive assay to quantify TH in both human and animal cells will provide a novel tool for further investigating possible PD immune regulatory pathways between brain and periphery.

The long lives of primates and the 'invariant rate of ageing' hypothesis.

Is it possible to slow the rate of ageing, or do biological constraints limit its plasticity? We test the 'invariant rate of ageing' hypothesis, which posits that the rate of ageing is relatively fixed within species, with a collection of 39 human and nonhuman primate datasets across seven genera. We first recapitulate, in nonhuman primates, the highly regular relationship between life expectancy and lifespan equality seen in humans. We next demonstrate that variation in the rate of ageing within genera is orders of magnitude smaller than variation in pre-adult and age-independent mortality. Finally, we demonstrate that changes in the rate of ageing, but not other mortality parameters, produce striking, species-atypical changes in mortality patterns. Our results support the invariant rate of ageing hypothesis, implying biological constraints on how much the human rate of ageing can be slowed.

Inward rectifier potassium channels in the HL-1 cardiomyocyte-derived cell line.

HL-1 is a line of immortalized cells of cardiomyocyte origin that are a useful complement to native cardiomyocytes in studies of cardiac gene regulation. Several types of ion channel have been identified in these cells, but not the physiologically important inward rectifier K(+) channels. Our aim was to identify and characterize inward rectifier K(+) channels in HL-1 cells. External Ba(2+) (100 µM) inhibited 44 ± 0.05% (mean ± s.e.m., n = 11) of inward current in whole-cell patch-clamp recordings. The reversal potential of the Ba(2+)-sensitive current shifted with external [K(+)] as expected for K(+)-selective channels. The slope conductance of the inward Ba(2+)-sensitive current increased with external [K(+)]. The apparent Kd for Ba(2+) was voltage dependent, ranging from 15 µM at -150 mV to 148 µM at -75 mV in 120 mM external K(+). This current was insensitive to 10 µM glybenclamide. A component of whole-cell current was sensitive to 150 µM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), although it did not correspond to the Ba(2+)-sensitive component. The effect of external 1 mM Cs(+) was similar to that of Ba(2+). Polymerase chain reaction using HL-1 cDNA as template and primers specific for the cardiac inward rectifier K(ir)2.1 produced a fragment of the expected size that was confirmed to be K(ir)2.1 by DNA sequencing. In conclusion, HL-1 cells express a current that is characteristic of cardiac inward rectifier K(+) channels, and express K(ir)2.1 mRNA. This cell line may have use as a system for studying inward rectifier gene regulation in a cardiomyocyte phenotype.

Kir 2.2 inward rectifier potassium channels are inhibited by an endogenous factor in Xenopus oocytes independently from the action of a mitochondrial uncoupler.

We previously showed inhibition of K(ir)2 inward rectifier K(+) channels expressed in Xenopus oocytes by the mitochondrial agents carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) and sodium azide. Mutagenesis studies suggested that FCCP may act via phosphatidylinositol 4,5-bisphosphate (PIP(2)) depletion. This mechanism could be reversible in intact cells but not in excised membrane patches which preclude PIP(2) regeneration. This prediction was tested by investigating the reversibility of the inhibition of K(ir)2.2 by FCCP in intact cells and excised patches. We also investigated the effect of FCCP on K(ir)2.2 expressed in human embryonic kidney (HEK) cells. K(ir)2.2 current, expressed in Xenopus oocytes, increased in inside-out patches from FCCP-treated and untreated oocytes. The fraction of total current that increased was 0.79 +/- 0.05 in control and 0.89 +/- 0.03 in 10 microM FCCP-treated (P > .05). Following "run-up," K(ir)2.2 current was re-inhibited by "cramming" inside-out patches into oocytes. Therefore, run-up reflected not reversal of inhibition by FCCP, but washout of an endogenous inhibitor. K(ir)2.2 current recovered in intact oocytes within 26.5 h of FCCP removal. Injection of oocytes with 0.1 U apyrase completely depleted ATP (P < .001) but did not inhibit K(ir)2.2 and inhibited K(ir)2.1 by 35% (P < .05). FCCP only partially reduced [ATP] (P < .001), despite inhibiting K(ir)2.2 by 75% (P < .01) but not K(ir)2.1. FCCP inhibited K(ir)2.2 expressed in HEK cells. The recovery of K(ir)2.2 from inhibition by FCCP requires intracellular components, but direct depletion of ATP does not reproduce the differential inhibitory effect of FCCP. Inhibition of K(ir)2.2 by FCCP is not unique to Xenopus oocytes.

Cytoplasmic domain structures of Kir2.1 and Kir3.1 show sites for modulating gating and rectification.

N- and C-terminal cytoplasmic domains of inwardly rectifying K (Kir) channels control the ion-permeation pathway through diverse interactions with small molecules and protein ligands in the cytoplasm. Two new crystal structures of the cytoplasmic domains of Kir2.1 (Kir2.1(L)) and the G protein-sensitive Kir3.1 (Kir3.1(S)) channels in the absence of PIP(2) show the cytoplasmic ion-permeation pathways occluded by four cytoplasmic loops that form a girdle around the central pore (G-loop). Significant flexibility of the pore-facing G-loop of Kir2.1(L) and Kir3.1(S) suggests a possible role as a diffusion barrier between cytoplasmic and transmembrane pores. Consistent with this, mutations of the G-loop disrupted gating or inward rectification. Structural comparison shows a di-aspartate cluster on the distal end of the cytoplasmic pore of Kir2.1(L) that is important for modulating inward rectification. Taken together, these results suggest the cytoplasmic domains of Kir channels undergo structural changes to modulate gating and inward rectification.

Ticagrelor versus clopidogrel in the management of acute myocardial infarction.

Hypothesis: In the care of acute myocardial infarction, ticagrelor attenuates post-ischemic myocardial damage and inhibits platelet activity to a greater extent than clopidogrel. Methods: Scholarly articles published in the last 10 years were compiled from a PubMed MeSH search focusing on acute coronary infarction and the antiplatelet therapies clopidogrel and ticagrelor. The databases used were PubMed, Google Scholar, Dynamed, and EBSCOhost. Eight articles were chosen based on subject matter related to the hypothesis, including cardioprotective effects, mortality benefits, platelet reactivity, angiographic effects, and electrocardiography changes. Results: Evidence from randomized clinical trials demonstrates that ticagrelor reduces infarct size, prevents remodeling, and reduces mortality rate after acute myocardial infarction to a greater extent than clopidogrel. However, some angiography studies show no difference between the two treatment regimes. Two articles show that ticagrelor is more effective in treating individuals with high platelet reactivity (HPR). In addition, there is some evidence of increased dyspnea and significant bleeding with ticagrelor. Discussion: Although there is growing evidence that ticagrelor is the better antiplatelet drug post-acute coronary infarction, more research needs to be done to determine the situations in which ticagrelor provides the optimal treatment regime in regards to cardioprotective effects, antiplatelet effects and an overall decrease in mortality. Conclusion: Ticagrelor was found to be superior to clopidogrel in relation to cardioprotective effects, mortality, and antiplatelet activity.

"To be healthy to me is to be free": how discourses of freedom are used to construct healthiness among young South African adults.

PURPOSE: Healthiness is constructed, in Western culture, as a moral ideal or supervalue. This paper will interrogate the assumption that health and the pursuit of healthiness is always and unquestionably positive, by exploring how discourses of health and freedom interact to reinforce the current inequalities and detract from social transformation. METHOD: Twenty young South African adults were interviewed about their understandings and experiences of health. These discussions were analysed using Foucauldian discourse analysis. RESULTS: Participants constructed healthiness as facilitating the experience of freedom, while at the same time being dependent on a personal orientation towards freedom (as opposed to merely submitting to dominant health authorities). Freedom discourses also played a role in connecting health to neoliberal discourses idealizing economic productivity and hard work. Participants were able to construct a self that is active, productive, valuable, hopeful, and self-assured when talking about health using discourses of freedom. However, these discourses also functioned to moralise and idealise healthiness, which contributed to blaming poor health on its sufferers. CONCLUSION: Health/freedom discourses can further reinforce the neoliberal value of individual responsibility by constructing self-improvement and self-work as the solution to ill-health, thereby contributing to victim-blaming and weakening support for public health interventions.