Financialization and the extractive industries:The case of South African platinum mining

This paper examines the impacts of financialization on corporate strategy in the extractive industries with a case study of South African platinum mining during the first two decades after apartheid. Drawing on insights from literature on financialization of the firm, the paper examines how intensified shareholder value pressures shaped strategy at major platinum mining companies during the long commodities boom of the 2000s and subsequent slump from 2009. The paper argues that financialization exacerbates the already intense cyclical volatility of the extractive industries. Efforts to fulfil narratives of shareholder value delivery during the boom manifested in large dividend distribution, gearing of balance sheets and aggressive outlays on capacity expansion and mergers and acquisition activity to demonstrate to the market an ambitious pipeline of growth projects. The result was financial fragility and excess capacity which has exacerbated the impact of the slump in subsequent years with severe social consequences. Distributional contest between management and organized labour has intensified as management has sought to restore internationally competitive rates of return on capital. The paper argues financialization of the firm in mining creates particularly acute distributional contestation and instability, due to the contradictions between the powerful abstractive tendencies of financialized capitalism and the social embeddedness of mining as a landed industry. The analysis has broader implications for the study of the extractive industries and development, and the political economy of post-apartheid South Africa

Adverse Health Outcomes in Relationship to Hypogonadism After Chemotherapy: A Multicenter Study of Testicular Cancer Survivors

Background: This study examined the prevalence of hypogonadism, its clinical and genetic risk factors, and its relationship to adverse health outcomes (AHOs) in North American testicular cancer survivors (TCS) after modern platinum-based chemotherapy. Patients and Methods: Eligible TCS were <55 years of age at diagnosis and treated with first-line platinum-based chemotherapy. Participants underwent physical examinations and completed questionnaires regarding 15 AHOs and health behaviors. Hypogonadism was defined as serum testosterone levels ≤3.0 ng/mL or use of testosterone replacement therapy. We investigated the role of 2 single nucleotide polymorphisms (rs6258 and rs12150660) in the sex hormone-binding globulin (SHBG) locus implicated in increased hypogonadism risk in the general population. Results: Of 491 TCS (median age at assessment, 38.2 years; range, 18.7–68.4 years), 38.5% had hypogonadism. Multivariable binary logistic regression analysis identified hypogonadism risk factors, including age at clinical evaluation (odds ratio [OR], 1.42 per 10-year increase; P=.006) and body mass index of 25 to <30 kg/m2 (OR, 2.08; P=.011) or ≥30 kg/m2 (OR, 2.36; P=.005) compared with <25 kg/m2. TCS with ≥2 risk alleles for the SHBG SNPs had a marginally significant increased hypogonadism risk (OR, 1.45; P=.09). Vigorous-intensity physical activity appeared protective (OR, 0.66; P=.07). Type of cisplatin-based chemotherapy regimen and socioeconomic factors did not correlate with hypogonadism. Compared with TCS without hypogonadism, those with hypogonadism were more likely to report ≥2 AHOs (65% vs 51%; P=.003), to take medications for hypercholesterolemia (20.1% vs 6.0%; P<.001) or hypertension (18.5% vs 10.6%; P=.013), and to report erectile dysfunction (19.6% vs 11.9%; P=.018) or peripheral neuropathy (30.7% vs 22.5%; P=.041). A marginally significant trend for increased use of prescription medications for either diabetes (5.8% vs 2.6%; P=.07) or anxiety/depression (14.8% vs 9.3%; P=.06) was observed. Conclusions: At a relatively young median age, more than one-third of TCS have hypogonadism, which is significantly associated with increased cardiovascular disease risk factors, and erectile dysfunction. Providers should screen TCS for hypogonadism and treat symptomatic patients

Characterization of cellular abnormalities due to loss of TSC2

Tuberous sclerosis complex (TSC) is a disorder characterized by multiple benign tumours in all major organs that can result in neurological manifestations including mental retardation and autism. TSC results from mutation in TSC1 or TSC2, which together form a complex that serves as a negative regulator of protein kinase mTORC1, a key regulator of cell growth and metabolism. Thus, cells with diminished TSC1:TSC2 function display elevated mTORC1 signaling, leading to the formation of benign tumours with very large cells. Rapamycin is a potent mTORC1 inhibitor, and rapamycin derivative everolimus has been approved for treatment of TSC patients with inoperable subependymal giant cell astrocytomas. However, these drugs can have serious side effects and should not be used for extended periods of time. In a screen of approved human drugs, amiodarone, dronedarone, perhexiline, and niclosamide were found to inhibit the elevated mTORC1 signaling seen in mouse embryo fibroblast (MEF) cells lacking TSC2. The goal of this project was to determine whether the many abnormal cell phenotypes associated with loss of TSC2 are directly related to elevated mTORC1 levels, and whether these drugs can ameliorate these abnormal phenotypes. Unlike wild type MEFs, TSC2-null MEFs showed an epithelial-like morphology with an increase in localization of actin to the cell periphery, focal adhesions, localization of β-catenin to cell-cell junctions, and localization of N-cadherin to cell-cell junctions. Exposure of TSC2-null MEFS to the mTORC1 inhibitors for seven days caused a transition from an epithelial-like to a fibroblast-like morphology in all of the aforementioned phenotypes, resembling that of wild type MEFs. TSC2-null MEFs were shown to express E-cadherin, a cell adhesion protein not normally found in MEFs. Knocking down levels of TSC2 in wild-type MEFs did not induce expression of E-cadherin, but restoring TSC2 expression in TSC2-null MEFs slightly reduced E-cadherin expression. A tentative model was proposed to explain how TSC2 can control E-cadherin expression, which has not yet been described in literature.Medicine, Faculty ofBiochemistry and Molecular Biology, Department ofGraduat

sierra: Sierra Platinum v1.0

Sierra Platinum v1.0: A Fast and Robust Optimal Multiple-Replicate Peak-Caller With Visual Quality-Control and -Steerin

[RETRACTED] Platinum Label Body Tone Keto -This Diet Supplement Really Work? v1

[RETRACTED]Platinum Label Body Tone Keto </p