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Home Cardiology Editor's Pick: Lipoprotein(a) and Calcific Aortic Valve Stenosis
Editor's Pick: Lipoprotein(a) and Calcific Aortic Valve Stenosis
17 October 2019 | Download as | PDF
Our Editor's pick for this year's edition of EMJ Cardiology is the review paper by Kosmas et al. which presents the role of the complex polymorphic lipoprotein(a) and its implication in calcific aortic valve stenosis. Studies have previously associated enhanced levels of lipoprotein(a) with increased risk of cardiovascular disease. This paper is a comprehensive review of the current data indicating the causative role of lipoprotein(a) in aortic valve calcification and aortic valve stenosis, and outlines the need for better understanding of the complex molecular processes to ultimately reduce calcific aortic valve stenosis morbidity and mortality.
*Constantine E. Kosmas,1 Delia Silverio,2 Andreas Sourlas,3 Frederick N. Campos,2 Peter D. Montan,2 Eliscer Guzman1
1. Department of Medicine, Montefiore Medical Center, Bronx, New York, USA
2. Cardiology Clinic, Cardiology Unlimited PC, New York City, New York, USA
3. School of Medicine, University of Crete, Heraklion, Greece
*Correspondence to [email protected]
Dr Kosmas and Dr Guzman have received speaking honoraria from Amgen as members of the Dyslipidemia Speaker Bureau.
EMJ Cardio. 2019;7[1]:89-97.
Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.
Calcific aortic valve stenosis is the most common valve disease in the elderly population and is associated with significant morbidity and mortality. This condition is characterised by gradual fibrosis, thickening, and calcification of the affected leaflets, leading to decreased leaflet mobility and increased obstruction of the blood flow from the left ventricle. Lipoprotein(a) [Lp(a)] is a complex polymorphic lipoprotein with proatherogenic, proinflammatory, and prothrombotic properties. Several epidemiologic and clinical studies have described elevated Lp(a) levels as an independent causative risk factor for cardiovascular disease, including coronary artery disease, stroke, peripheral artery disease, heart failure, and venous thromboembolism. On the other hand, several studies have also described Lp(a) as a strong genetic causative risk factor for aortic valve calcification and aortic valve stenosis. In this review, the authors present and discuss the scientific and clinical evidence pertaining to the role of Lp(a) in calcific aortic valve stenosis.
Lipoprotein(a) [Lp(a)] is a complex polymorphic lipoprotein synthesised by the liver. Lp(a) presents a similar structure with the low-density lipoprotein (LDL) molecule, only differing in the presence of the glycoprotein apolipoprotein(a) [(Apo(a)], which is covalently bound via a disulfide bond to the apolipoprotein B-100 (ApoB-100) of the LDL molecule.1 More specifically, Lp(a) comprises one molecule of an ApoB-100-containing LDL particle and one molecule of a large, highly polymorphic glycoprotein called Apo(a). A distinctive feature of Apo(a) is the presence of triple loop structures, which are called kringles. Kringle domains are stabilised by three internal disulfide bonds and are also found in certain coagulation factors, such as plasminogen, tissue plasminogen activators, prothrombin, and urokinase. However, in contrast to plasminogen, the linker sequences that join individual kringles are glycosylated in Apo(a). The two main components of Lp(a) are covalently linked together via a disulfide bond between the ApoB-100 of the LDL moiety and one of the kringle domains in Apo(a).2
Plasma levels of Lp(a) are under strict genetic control mainly by the LPA gene, largely unaffected by food intake, type of diet, presence of inflammation, or environmental factors.1,3 While the physiological role of the Lp(a) has not yet been well elucidated, this lipoprotein has been associated with several physiological processes, such as wound healing and tissue repair, as well as inhibition of cancer growth and spread.4 There is extensive evidence demonstrating that Lp(a) presents proatherogenic, proinflammatory, and prothrombotic properties, because it promotes the oxidation of LDL, enhances secretion and expression of proinflammatory cytokines, promotes platelet aggregation, and impairs plasminogen activation.5-8 Lp(a) is currently considered as an independent genetic, causative risk factor for cardiovascular disease (CVD), including coronary artery disease (CAD),9-11 stroke,10,11 peripheral artery disease,11 heart failure,12 and venous thromboembolism.13 In addition, several studies have also described Lp(a) as a strong causative risk factor for aortic valve calcification (AVC) and aortic valve stenosis (AVS).14-16
Calcific AVS (CAVS) is the most common valve disease in the elderly population, affecting >1 million patients in the USA, and is associated with significant morbidity and mortality.17 In Norway, the prevalence of AVS is also consistently increasing with age, average values being 0.2% in the 50–59 year old cohort, 1.3% in the 60–69 year old cohort, 3.9% in the 70–79 year old cohort, and 9.8% in the 80–89 year old cohort.18 In Sweden, the age-adjusted incidence of AVS declined from 15.0 to 11.4 in men and 9.8 to 7.1 in women per 100,000 from 1989–1991 and 2007–2009, and the median age at diagnosis increased by 4 years for both men and women.19 In a large systematic review and meta-analysis of population-based studies from 19 European countries and North America, the pooled prevalence of all AVS in the elderly (>75 years) was 12.4% and the prevalence of severe AVS was 3.4%.20 CAVS is characterised by gradual fibrosis, thickening, and calcification of the affected leaflets, thus leading to decreased leaflet mobility and increased obstruction of the blood flow from the left ventricle.17,21
The pathogenesis of AVS shares many similarities to that of atherosclerosis. Several longitudinal studies have demonstrated that hypercholesterolaemia has a significant impact on the development of degenerative AVS. Notwithstanding, in several clinical studies, intensive statin therapy has failed to halt the progression of CAVS or induce its regression.22-24 Here, it should be noted that statins have been shown to increase Lp(a) levels by roughly 10–20%,6,25,26 which could be one explanation as to why statins were proven ineffective in halting the progression of CAVS. In contrast, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have been shown to reduce Lp(a) levels by 24.5–29.5%.27 Related to this, it was recently shown that high levels of PCSK9 predicted development of AVS requiring surgery, although this association seemed to be driven by concurrent atherosclerotic disease.28
On the other hand, AVS hasalso been associated with several other atherogenic risk factors, such as diabetes, hypertension, smoking, male sex, as well as age, apparently due to progressive fibro-calcific remodeling.29 In addition, there are data indicating that chronic Chlamydia pneumoniae infection may act as a 'trigger' and aggravate AVS via the formation of circulating immune complexes. Importantly, a strong synergism was also observed between Lp(a) and C. pneumoniae IgG antibodies in circulating immune complexes.30 In this review, the authors aim to present and discuss the scientific and clinical evidence pertaining to the role of Lp(a) in CAVS.
STUDY EVIDENCE PERTAINING TO THE ROLE OF LIPOPROTEIN(a) IN AORTIC VALVE CALCIFICATION AND STENOSIS
There is extensive evidence from genetic and clinical studies demonstrating the causative association of elevated Lp(a) with CAVS.
Studies Establishing the Association of Aortic Valve Calcification and Stenosis with Increased Lipoprotein(a) Levels
The first report to demonstrate an association between Lp(a) and AVS was published in 1995. The study showed that AVS was present in 36.1% of subjects with Lp(a) levels ≥30.0 mg/dL, but only in 12.7% of subjects with Lp(a) levels <30.0 mg/dL (p<0.001).31
In another study, which evaluated the role of novel coronary risk factors in the development of AVC, it was clearly demonstrated that patients with AVC had significantly higher serum Lp(a) levels, as compared with subjects with essentially normal aortic valve morphology (27.4 mg/dL versus 19.9 mg/dL, respectively; p=0.033). Moreover, multivariate analysis identified Lp(a) as an independent predictor of AVC.32
Study Evaluating the Impact of Increased Lipoprotein(a) Levels on Aortic Valve Calcification in Patients with Familial Hypercholesterolaemia
Patients with familial hypercholesterolaemia (FH) have been shown to have a higher prevalence and extent of AVC than patients with non-familial hypercholesterolaemia.33 Exposure to classical risk factors alone cannot adequately explain the onset and progression of AVC in statin-treated FH patients.34 On the other hand, patients with FH have been shown to have 3-fold higher plasma Lp(a) levels than controls, apparently due to variation at the LDL receptor gene locus.35 Thus, in a study, which included 129 asymptomatic statin-treated patients with FH, and was designed to investigate whether Lp(a) concentration is associated with AVC in this cohort of patients, Vongpromek et al.34 showed that for a 10 mg/dL increase in Lp(a) concentration in those patients, there was an 11% associated increased risk of developing AVC. Multivariate analysis again identified Lp(a) as a significant independent predictor of AVC. Of note, however, Lp(a) levels were not associated with the presence or severity of coronary artery calcification.34
Genetic Studies
Genome-wide association studies (GWAS) are designed to test the association between markers, called single-nucleotide polymorphisms (SNP), across the genome and disease, usually involving ≥300,000 markers that are reasonably polymorphic and are spread across the genome fairly evenly.36 In other words, GWAS compare common genetic variants in large numbers of affected cases to those in unaffected controls to determine whether an association with disease exists.37 GWAS have been proven to be extremely useful in determining the association between elevated Lp(a) levels and CAVS.
In a GWAS, a SNP, rs10455872, in the LPA locus, encoding for Apo(a), was found to be significantly correlated with AVC (odds ratio [OR] per allele: 2.05). Importantly, the association between rs10455872 and Lp(a) levels was confirmed and it was clearly shown that Lp(a) levels mediate the effect of this SNP on AVC. Furthermore, in prospective analyses, LPA genotype was associated with incident AVS (hazard ratio [HR] per allele: 1.68) and aortic valve replacement (AVR) (HR: 1.54).14
In another study, which combined data from two prospective general population studies (the Copenhagen City Heart Study and the Copenhagen General Population Study), evaluating a total of 77,680 Danish individuals for as long as 20 years, elevated Lp(a) levels and corresponding LPA genotypes (rs10455872, rs3798220, kringle IV Type 2 [KIV-2] repeat polymorphism) were associated with an increased risk of AVS in the general population. More specifically, Lp(a) levels of 5–19 mg/dL, 20–64 mg/dL, 65–90 mg/dL, and >90 mg/dL were associated with multivariable adjusted HR for AVS of 1.2, 1.6, 2.0, and 2.9, respectively, as compared to levels of Lp(a) <5 mg/dL.15 Notably, the risk of AVS appears to increase continually as Lp(a) levels increase. In a large retrospective analysis, which assessed the correlation between Lp(a) levels and the incidence of AVS among patients with extremely high Lp(a) levels (>150 mg/dL), the prevalence of AVS was 3.74 times higher in the patients with Lp(a) levels >150.0 mg/dL, compared with those with Lp(a) levels <30.0 mg/dL.38
Furthermore, in a similar study, which used a multidirectional Mendelian randomisation approach and included 100,578 individuals from the general Danish population, elevated levels of Lp(a) were once again causally associated with increased risk of AVS. More specifically, a one-standard deviation (SD) increase in Lp(a) levels was associated observationally with a multifactorially adjusted HR of 1.23, whereas the corresponding causal risk ratios based on LPA SNP and on LPA KIV-2 genotype were 1.38 and 1.21, respectively. Of note, in this study, elevated Lp(a) levels were not causally associated with increased low-grade inflammation, as measured through levels of C-reactive protein (CRP).39
In another prospective Mendelian randomisation study, in which serum Lp(a) levels were measured in 17,553 participants of the European Prospective Investigation into Cancer (EPIC)-Norfolk study, elevated Lp(a) levels were associated with increased risk of AVS. More specifically, after adjusting for age, sex, and smoking history, participants in the top Lp(a) tertile had a 57% higher risk of AVS, as compared with those in the bottom Lp(a) tertile. Furthermore, heterozygotes and homozygotes for the rs10455872 genetic variant in the LPA locus were at increased risk for AVS with HR of 1.78 and 4.83, respectively, as compared to the individuals that did not carry the abnormal variant.40 These results were corroborated by a more recent, large case-control study, which replicated the association between LPA variants with AVS and showed a per risk allele OR of 1.34 for rs10455872 and 1.31 for rs3798220. Compared with individuals with no risk alleles, the homozygous OR for AVS was 2.05 for rs10455872 and 3.74 for rs3798220, while compound heterozygotes had a 2.00 OR for AVS.41
Studies Evaluating the Impact of Lipoprotein(a) and its Oxidised Phospholipid Content on Aortic Valve Calcification and Stenosis
In a study evaluating the impact of Lp(a) and oxidised phospholipids (OxPL) on ApoB-100 (OxPL-apoB), reflecting the biological activity of Lp(a), on AVS progression in 220 patients with mild-to-moderate AVS, elevated levels of Lp(a) and OxPL-apoB were associated with faster AVS progression and need for AVR. Based on the results of this study, the authors concluded that Lp(a) may mediate AVS progression through its associated OxPL.16 Of note, however, among patients with age ≤57 years, progression of AVS was 2-fold faster in those in the top Lp(a) tertile, as compared with those in the middle and bottom tertiles, whereas, in patients aged >57 years, the rate of AVS progression did not differ according to levels of Lp(a).16 This finding was corroborated in another more recent trial, in which for patients aged ≥70 years the development of AVS was not influenced by Lp(a) levels.42
In a secondary analysis of a randomised clinical trial, which included participants with mild-to-moderate CAVS with no indication for statin therapy from the ASTRONOMER (Effects of Rosuvastatin on Aortic Stenosis Progression) trial, the association of Lp(a) levels and its OxPL content with faster CAVS progression was actually linear. The results of this study reinforce the concept that measurement of Lp(a) levels should be performed in patients with mild-to-moderate CAVS to improve risk stratification and management.43
Studies Evaluating the Impact of Increased Lipoprotein(a) Levels on Aortic Valve Calcification and Stenosis in Patients with Bicuspid Aortic Valve
There is evidence suggesting that increased levels of Lp(a) are associated with the presence and severity of AVC in patients with bicuspid aortic valve (BAV). In an observational study, which looked at a small series of asymptomatic individuals with BAV, all the BAV subjects without AVC had normal Lp(a) levels, whereas 75% (3 out of 4) of cases with AVC had elevated Lp(a) levels. Although the author recognised that this was only a small series of BAV cases, notwithstanding, it was suggested that the concept that the plasma Lp(a) concentration may play a major role in the calcification process of the BAV would be worth exploring in larger samples.44 Later on, this concept was corroborated in another larger study, which investigated the association of Lp(a) and LPA KIV-2 repeat number with the presence of calcification and stenosis in patients with BAV. In that study, among BAV patients there was a clear positive association between Lp(a) levels and the degree of AVC. In contrast, lower LPA KIV-2 repeat numbers were observed in subjects with more severe AVC. Based on the results of this study, the authors suggested that Lp(a) may serve as a risk marker for the identification of BAV patients most likely to develop AVC and AVS.45 However, the potential effect of lowering Lp(a) on the development and progression of AVC in patients with BAV would need to be further investigated in larger randomised controlled trials.
Studies Addressing the Question Whether the Association of Elevated Lipoprotein(a) Levels with Aortic Valve Calcification and Stenosis is Dependent upon the Concomitant Presence of Coronary Artery Disease
As previously discussed, Lp(a) is considered an independent genetic, causative risk factor for CAD. Thus, the question may be raised whether the association of elevated Lp(a) with CAVS is dependent upon, or mediated by, the concomitant presence of CAD. In a nested, case-referent study, high Lp(a) levels and a high Apo B/A1 ratio were associated with surgery for AVS in patients with concomitant CAD, but not in those with isolated AVS (without concomitant CAD).46 However, in a more recent large genetic association study, genetically elevated Lp(a) levels were associated with CAVS independently of the presence of CAD, and individuals with high Lp(a) levels had a significantly increased risk for CAVS even in the absence of CAD. Based on the results of this study, the authors suggested that the measurement of Lp(a) levels in patients with CAVS might be proven clinically useful.47
POTENTIAL MECHANISMS THROUGH WHICH ELEVATED LIPOPROTEIN(a) MAY LEAD TO CALCIFIC AORTIC VALVE STENOSIS
As previously discussed, CAVS is the most common valve disease in the elderly population and its pathogenesis shares many similarities to that of atherosclerosis. Researchers have described an 'early lesion' that shared common histologic features with the early lesion of atherosclerotic plaques, suggesting that CAVS could be an atherosclerotic disease.21 Studies indicate that inflammation, lipid deposition, and fibrosis, which are all important contributors to atherogenesis, also play an important role in the pathogenesis and progression of CAVS.48,49 Lp(a) is a major carrier of proinflammatory OxPL.5 OxPL co-localise with Lp(a) in arterial and aortic valve lesions and thus may be directly involved in the pathogenesis of CVD and CAVS by promoting endothelial dysfunction, lipid deposition, inflammation, and osteogenic differentiation, leading to calcification. Thus, OxPL may potentially provide a mechanistic link between CVD and CAVS.50 In view of the similarities shared in the pathogenesis of atherosclerosis and CAVS, it can become easily understandable that molecules promoting inflammation and atherosclerosis, such as Lp(a), may also have a direct impact on CAVS.
Even though the precise mechanism by which Lp(a) promotes the initiation and progression of CAVS has not been clearly elucidated, there are multiple proposed mechanisms through which elevated Lp(a) levels may lead to CAVS. Similar to LDL, transfer of Lp(a) from the circulation into the arterial intima and aortic valve cusps leads to cholesterol deposition with subsequent thickening of the aortic valve cusps.51
On the other hand, Lp(a) has been shown to trigger apoptosis in endoplasmic reticulum-stressed macrophages via a mechanism requiring both cluster of differentiation 36 (CD36) and toll-like receptor 2 (TLR2). This macrophage apoptosis may signify a key process, likely contributing to early valvular lesion progression.52,53
Furthermore, as it was mentioned earlier, Lp(a) exhibits prothrombotic properties because it competes with plasminogen and therefore prevents plasmin from dissolving fibrin clots,6-8 thus leading to fibrin deposition on the aortic leaflets and subsequent progression of AVS.51
Lp(a) is involved in the wound-healing process and may accumulate at sites of injury3 promoting cholesterol deposition. Thus, it may be well contemplated that accumulation of Lp(a) at sites of minor injury, such as the affected aortic leaflets at the very initial stages of AVS, may lead to increased cholesterol and thrombi deposition, thus promoting the progression of AVS.51
Finally, another molecule that has been implicated is autotaxin (ATX), a lysophospholipase D enzyme, which transforms lysophosphatidylcholine into lysophosphatidic acid (LysoPA). ATX is transported in the aortic valve via the bloodstream by Lp(a) and is also secreted by valve interstitial cells. ATX-LysoPA has been shown to promote inflammation and mineralisation of the aortic valve, thus promoting CAVS.54 More specifically, pericellular LysoPA may associate with lysophosphatidic acid receptor 1 (LPAR1), which promotes nuclear translocation of NF-κB. The activation of NF-κB leads to an increased expression of IL-6 and bone morphogenetic protein 2 (BMP-2), which are known pro-osteogenic factors.55
A schematic of the potential mechanisms through which elevated Lp(a) may lead to CAVS is shown in Figure 1.
Figure 1: Potential mechanisms through which elevated lipoprotein(a) may lead to calcific aortic valve stenosis. ATX: autotaxin; CAVS: calcific aortic valve stenosis; ER: endoplasmic reticulum.
PRELIMINARY EVIDENCE PERTAINING TO THE EFFECT OF LIPOPROTEIN(a) LOWERING ON THE RISK OF AORTIC VALVE CALCIFICATION AND STENOSIS
In an elegant study, which used human aortic valve interstitial cells (HAVIC), it was clearly demonstrated, for the first time, that Lp(a) is causally involved in the induction of AVC. It was also shown that the LPA gene is locally expressed in the stenotic aortic valve. Lp(a) was found to induce osteogenic differentiation of HAVIC via induction of the gene encoding for the tissue-nonspecific alkaline phosphatase, as well as certain pro-osteogenic mediators. Moreover, it was shown that the Lp(a)-induced osteogenic differentiation of HAVIC was associated with an increase in the phosphorylation of several kinases implicated in cellular remodelling and apoptosis, such as mitogen-activated protein kinase-38 (MAPK38) and glycogen synthase kinase-3 beta (GSK3β). Inhibition of MAPK38 or GSK3β led to a significant reduction of Lp(a)-induced HAVIC calcification. Thus, interfering with the Lp(a) pathway could provide a novel therapeutic approach for the prevention or even reversal of CAVS.56
In another multimodality imaging study, Lp(a) and OxPL promoted valve calcification in patients with AVS. In this study, Lp(a) and OxPL-apoB levels were measured in 145 patients with AVS. Initially, on baseline 18F-sodium fluoride PET (18F-NaF PET), patients in the top Lp(a) tertile (>35.0 mg/dL) had increased valve calcification activity compared with those in the lower tertiles. Moreover, during follow-up, patients in the top Lp(a) tertile demonstrated increased progression of valvular CT-obtained calcium score, faster haemodynamic progression on echocardiography, and an increased incidence of AVR and death compared with those in the lower tertiles. Similar results were observed with OxPL-apoB. In vitro, Lp(a) induced osteogenic differentiation of HAVIC through its OxPL content. The Lp(a)-induced osteogenic differentiation of HAVIC was considerably attenuated with the E06 monoclonal antibody against OxPL. Again, these findings clearly demonstrate that elevated Lp(a) and OxPL-apoB levels promote AVC, and lowering Lp(a) or inactivating OxPL may potentially lead to slowing of AVC. Thus, these findings suggest that therapeutic approaches reducing elevated Lp(a) and OxPL levels in patients with AVS could slow disease progression and delay the need for AVR.57
Although to date no clinical trials have been conducted to assess the impact of Lp(a) lowering on the incidence of AVS, an analysis using data from a large prospective European cohort has shown that lowering Lp(a) to <50.0 mg/dL in the general population would be theoretically expected to reduce the overall incidence of AVS by 13.9%.58
The above review of the scientific, epidemiological and clinical data clearly demonstrates that Lp(a) plays an independent causative role in CAVS.However, additional evidence is needed to help us better understand the precise molecular mechanisms by which elevated Lp(a) causes CAVS and promotes its progression. Furthermore, it remains to be seen if pharmaceutical interventions that decrease Lp(a) levels would also be clinically effective in reducing the risk of CAVS and its associated morbidity and mortality.
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J Clin Endocrinol Metab. 2015;100(7):2690-9. Arsenault BJ et al. Lipoprotein(a) levels, genotype, and incident aortic valve stenosis: A prospective Mendelian randomization study and replication in a case-control cohort. Circ Cardiovasc Genet. 2014;7(3): 304-10. Chen HY et al. Association of LPA variants with aortic stenosis: A large-scale study using diagnostic and procedural codes from electronic health records. JAMA Cardiol. 2018;3(1):18-23. Mahabadi AA et al. Comparison of lipoprotein(a)-levels in patients ≥70 years of age with versus without aortic valve stenosis. Am J Cardiol. 2018;122(4):645-49. Capoulade R et al. Association of mild to moderate aortic valve stenosis progression with higher lipoprotein(a) and oxidized phospholipid levels: Secondary analysis of a randomized clinical trial. JAMA Cardiol. 2018;3(12):1212-7. [Epub ahead of print]. Ker J. Bicuspid aortic valve disease and lipoprotein(a)--A concept worth exploring? Int J Cardiol. 2014;174(1):197-203. Sticchi E et al. Role of lipoprotein (a) and LPA KIV2 repeat polymorphism in bicuspid aortic valve stenosis and calcification: A proof of concept study. Intern Emerg Med. 2019;14(1):45-50. Ljungberg J et al. Lipoprotein(a) and the apolipoprotein B/A1 ratio independently associate with surgery for aortic stenosis only in patients with concomitant coronary artery disease. J Am Heart Assoc. 2017;6(12).pii:e007160. Perrot N et al. Genetic variation in LPA, calcific aortic valve stenosis in patients undergoing cardiac surgery, and familial risk of aortic valve microcalcification. JAMA Cardiol. 2019;4(7):620-7. [Epub ahead of print]. Coté N et al. Inflammation is associated with the remodeling of calcific aortic valve disease. Inflammation. 2013;36(3):573-81. Parisi V et al. The lipid theory in the pathogenesis of calcific aortic stenosis. Nutr Metab Cardiovasc Dis. 2015;25(6):519-25. Boffa MB, Koschinsky ML. Oxidized phospholipids as a unifying theory for lipoprotein(a) and cardiovascular disease. Nat Rev Cardiol. 2019;16(5):305-18. Nordestgaard BG, Langsted A. How does elevated lipoprotein(a) cause aortic valve stenosis? J Am Coll Cardiol. 2015;66(11):1247-9. Seimon TA et al. Atherogenic lipids and lipoproteins trigger CD36-TLR2-dependent apoptosis in macrophages undergoing endoplasmic reticulum stress. Cell Metab. 2010;12(5):467-82. Thanassoulis G. Lipoprotein (a) in calcific aortic valve disease: From genomics to novel drug target for aortic stenosis. J Lipid Res. 2016;57(6):917-24. Bouchareb R et al. Autotaxin derived from lipoprotein(a) and valve interstitial cells promotes inflammation and mineralization of the aortic valve. Circulation. 2015;132(8):677-90. Mathieu P, Boulanger MC. Autotaxin and lipoprotein metabolism in calcific aortic valve disease. Front Cardiovasc Med. 2019;6:18. Yu B et al. Lipoprotein(a) induces human aortic valve interstitial cell calcification. JACC Basic Transl Sci. 2017;2(4):358-71. Zheng KH et al. Lipoprotein(a) and oxidized phospholipids promote valve calcification in patients with aortic stenosis. J Am Coll Cardiol. 2019;73(17):2150-62. Afshar M et al. Estimating the population impact of Lp(a) lowering on the incidence of myocardial infarction and aortic stenosis-brief report. Arterioscler Thromb Vasc Biol. 2016;36(12):2421-3.
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Q: Why can't Box be used as an associated type which needs to implement T? I'd like to use Box<dyn std::error::Error> as an associated type which needs to implement std::error::Error:
trait Foo {
    type Error: std::error::Error;
}

struct Bar();

impl Foo for Bar {
    type Error = Box<dyn std::error::Error>;
}

Rust Playground
However, this does not seem to work:
error[E0277]: the size for values of type `(dyn std::error::Error + 'static)` cannot be known at compilation time
 --> src/lib.rs:8:18
  |
1 | trait Foo {
  |       --- required by a bound in this
2 |     type Error: std::error::Error;
  |                 ----------------- required by this bound in `Foo`
...
8 |     type Error = Box<dyn std::error::Error>;
  |                  ^^^^^^^^^^^^^^^^^^^^^^^^^^ doesn't have a size known at compile-time
  |
  = help: the trait `std::marker::Sized` is not implemented for `(dyn std::error::Error + 'static)`
  = note: required because of the requirements on the impl of `std::error::Error` for `std::boxed::Box<(dyn std::error::Error + 'static)>`

As far as I understood the documentation, Box<T> implements std::error::Error if T does it. I also tried to create a custom trait SizedError: std::error::Error + Sized and use a Box<dyn SizedError> but that doesn't help either.
Is there any way I can set Foo::Error such that I can return any error?

redpajama_set_name: RedPajamaStackExchange


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DC Is Introducing a Weird New Multiverse in Dark Nights: Metal
Scott Snyder
Greg Capullo
Image: DC Comics. Art by Greg Capullo
DC's next big event, Dark Nights: Metal, is promising to head to some strange places. How strange? "The Justice League clad in '90s action figure armor plating fighting in an alien combat arena" strange. And honestly, it sounds kind of great.
Scott Snyder, former Batman writer and part of the team behind Dark Nights: Metal, discussed the upcoming series with IGN today. While doing so, he revealed that the series has some seriously wild ties to the arcane world of DC's cosmology, linking Hawkman's own research into Nth Metal—a material that's been in existence in the DC universe since the origin of reality itself—to an experiment by Batman. It seemingly sees the Justice League discover a whole new multiverse, just hiding beneath the reality DC's heroes usually inhabit:
I can't say too much about it. I don't want to spoil too much, but ultimately, I got fascinated by this idea that our universe itself is comprised mostly of dark matter and dark energy. Things that we can't perceive at all, and we've only discovered that relatively recently. So it's almost as if our universe is the foam on the ocean of things that we can't see, or know, or perceive, and yet we feel the affects of those things right and left.
The Dark Multiverse is sort of a completely unexplored area of the DC cosmology that's new to it, but fits in with the cosmology that's been created by all of the writers and artists ahead of me. In terms of what Grant [Morrison] was able to do in Multiversity, with Geoff Johns in Infinite Crisis and all the way down to stories like Cosmic Odyssey. I had a great time re-reading all of that stuff.
Basically, stuff is going to get weird. And not just dark for the sake of it. Despite the name and the above art of the Justice League, which wouldn't look out of place painted onto the side of a van in the mid '90s, Snyder sees this event, something he'd been laying hints out for in his seminal run on Batman with Greg Capullo, as an exploration of new and exciting material for DC, while Rebirth focuses on restoring nostalgic vibes to the company's roster of heroes:
I would spoil so much if I answered that. What I'll say about the Dark Multiverse is that if Rebirth – which has been so good to us and Geoff Johns did such a great job with – is largely about bringing back classic, restoring legacy and honoring the great characters from the past and bringing them back in a way to set them up, then Metal gets to be the bad brother. The one that gets to create all kinds of new stuff. I can say that it affects, or at least the properties of dark energy, dark matter and begin to affect the DCU.
Teaser art by Andy Kubert for the new Challengers and Sideways series, debuted at C2E2 earlier this year.
While we don't know how this new universe will affect Wonder Woman, Batman, Superman, and the rest of DC's heroes quite yet, we do know it's bringing some familiar superteams and new characters with it in a new Dark Matter line that will spin out of Metal, featuring five new series in the form of The Silencer, Sideways, The Immortal Men, Damage, and New Challengers. But so far, Metal sounds like it's going to be experimenting with some truly out-there elements of the DC cosmic that I can't wait to see someone like Snyder tackle.
Dark Nights: Metal is set to begin later this year.
[IGN]
Superman and Watchmen's Dr. Manhattan Will Clash in Doomsday Clock
There's Gonna Be a Whole Lot of Batman in DC Comics' Next Big Event
New Mister Miracle Comic Will Explore the Tragic Irony of Jack Kirby's Escape Artist Jesus
James is a News Editor at io9. He wants pictures. Pictures of Spider-Man!

redpajama_set_name: RedPajamaCommonCrawl


e-Strategy Trends' continually updated collection of trends and statistics about trust for marketing, public relations, advertising and strategic communications professionals.
Some 55% of surveyed consumers say they are mostly willing to share information with retailers in order to get a better shopping experience, and 57% say they are somewhat willing to do so.
Search results influence consumers' perceptions about a company, according to 81% of the respondents worldwide in a November 2011 study.
Three-quarters of consumers said they were very (33%) or somewhat (42%) likely to respond to a brand offer reposted by a friend.
Consumers also had their trust in a brand boosted by mobile content that went beyond a sales message to provide them with some utility.
84% of US consumers felt that brands needed to prove themselves trustworthy before they would interact with them or other information sources.
HubSpot analyzed nearly 9 million Twitter profiles to produce this graph about the effect a photo has on a social media profile in gaining followers.
Consumers who are aware of Facebook's use of their profile information and posts to target ads towards them aren't very accepting of this practice.
Only a minority of US consumers have complete trust that companies protect their personal information online, according to the Q2 2012 TRUSTe Privacy Index.


Rio Lagartos - On the northern shore of the peninsula, Río Lagartos (Alligator River) is a fishing village that also boasts the densest concentration of pink Caribbean flamingoes in Mexico; approximately 40,000 have been registered.
Within the Ría Lagartos Biosphere Reserve, a mangrove-lined estuary, are 395 bird species as well as the crocodiles that gave the town its name.
Less than a half mile east of the town is Las Coloradas, a little known part of Yucatán, with picturesque and unordinary landscapes, a giant salt factory and amazing pink lagoons.
9:15 - 12:15 - Boat tour to observe the amazing spectacle of hundreds of Pink Flamingoes. On the way, you will observe a great variety of aquatic birds and crocodiles in their natural habitat; the tour includes a stop in La Colorada where its waters are pink ... Yes! we said pink water, and it is just unbelievable! Following, you can have a "bano Maya" (Mayan bath) with white clay mud that is fantastic for the skin; finally, you will have swim time at a nearby beach or in a fresh water spring.
We toured the river on a small boat and it was a perfect day!! The river is so calm with tons of wildlife. We just found a guide while coming into town. We stopped at the pink lakes! and got a mayan mud bath with the mineral enriched mud. Then it ended at a gorgeous blue beach to rinse off and enjoy a swim.


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Tag: Karen Gillan
Director: Michael Dowse Starring: Dave Bautista, Kumail Nanjiani, Mira Sorvino, Natalie Morales, Iko Uwais, Betty Gilpin, Karen Gillan, Jimmy Tatro, Steve Howey Written by Tripper Clancy Running Time: 93 mins Cert: 15 Release date: 12th July 2019 Stuber is a real throwback to those buddy cop films that were nineteen to the dozen in the…
Director: Anthony Russo and Joe Russo Starring: Robert Downey Jr, Chris Evans, Chris Hemsworth, Scarlett Johansson, Mark Ruffalo, Jeremy Renner, Don Cheadle, Paul Rudd, Brie Larson, Karen Gillan, Josh Brolin, Danai Gurira, Bradley Cooper, Gwyneth Paltrow Written by Christopher Markus, Stephen McFeely, (based on the Marvel comics) Stan Lee, Jack Kirby and (comic book) Jim…
Directors: Anthony Russo and Joe Russo Starring: Robert Downey Jr, Chris Hemsworth, Chris Evans, Scarlet Johanssen, Mark Ruffalo, Benedict Cumberbatch, Chris Pratt, Don Cheadle, Tom Holland, Chadwick Boseman, Josh Brolin, Zoe Saldana, Karen Gillan, Tom Hiddleston, Paul Bettany, Elizabeth Olsen, Anthony Mackie, Sebastian Stan, Idris Elba, Danai Gurira, Benedict Wong, David Bautista, Pom Klementieff, Vin…
Director: Jake Kasdan Starring: Dwayne Johnson, Kevin Hart, Jack Black, Karen Gillan, Rhys Darby, Bobby Cannavale, Nick Jonas, Alex Wolff, Ser'Darius Blain, Madison Iseman, Morgan Turner Written by: Erik Sommers, Scott Rosenberg, Jeff Pinker, (also story) Chris McKenna and (based on the book "Jumanji" ) Chris Van Allsburg Running Time: 119 mins Cert: 12A Release…
Director: James Gunn Starring: Chris Pratt, Zoe Saldana, Dave Bautista, Vin Diesel, Bradley Cooper, Michael Rooker, Karen Gillan, Pom Klementieff, Kurt Russell, Elizabeth Debicki, Sylvester Stallone. Written by: James Gunn, (based on the Marvel comics) Dan Abnett and Andy Lanning Running Time: 136 mins Cert: 12A Release date: 28th April 2017 Guardians of the Galaxy…
Director: James Gunn Starring: Chris Pratt, Zoe Saldana, Dave Bautisia, Vin Diesel, Bradley Cooper, Glenn Close, John C. Reilly, Karen Gillan, Lee Pace Written by: James Gunn, Nicole Perlman, (based on the comic book) Dan Abnett and Andy Lanning Running Time: 121 mins Cert: 12A Release date: 31st July 2014 Marvel's newest entry in the…
Director: Mike Flanagan Starring: Karen Gillan, Brenton Thwaites, Katee Sackhoff, Rory Cochrane, Annalise Basso, Garrett Ryan Written by: Jeff Howard, (also based on a short screenplay) Mike Flanagan and (based on a short screenplay) Jeff Seidman Running Time: 104 mins Cert: 15 Release date: 13th June 2014 At last! A modern horror film that doesn't rely on the…


text:
"Hill of Hell" by Laura van den Berg published in Virginia Quarterly Review
A haunting and delicately written story about family, secrets, and how quickly life passes. Check it out here: "Hill of Hell" by Laura van den Berg published in 2019.
The story starts in a rather mundane way: two friends reunite after a three year absence. The one friend, a professor, invites the narrator to give a lecture at the college where he teaches. Afterward, they drink, they converse, they ride the train together. Nothing extraordinary, except at one point we learn of the narrator's recent pregnancy resulting in a still born birth. That, and, "Our marriage is on borrowed time," the narrator tells her friend. A moment later, in the same conversation, we learn of the narrator's friend's philosophy of "the big alone" which allows us a short cut into the friend's world view: in the end, we have no one, nothing. All the while, thoughout the train ride, we glimpse specific moments and physical details: a sweaty brow, a memory of Ikea, a dream, the conductor brandishing a photo of his child, a bottle of wine, a newspaper.
The next section moves us forward in time: "Six months after my friend and I rode the train together, I left my husband. Some years later, I remarried. My friend was invited to the wedding, but he was too ill to attend. He sent me a note of congratulations and that was the last time I heard from him before he died. In my second marriage, I was the one who lobbied for a child and when I gave birth to a daughter…"
Say what? In five brief sentences, we witness divorce, remarriage, death, and birth. Perhaps the most ambitious set of lines in all of fiction?
What follows is a rendering of two parents and their daughter and the evolution of their relationship through tears and hardships. The narrator even acknowledges: "It pains me to say that our daughter was, from the moment of her birth, a difficult human being."
I've often wondered what constitutes "a difficult human." After all, aren't we all in our own ways difficult? Even those who attempt pleasantries at all costs have their difficulties. Perhaps they're the most difficult of all, at least on the surface.
In any case, we move from the scene on the train to an overview of the narrator's daughter who has lived a life mostly away from her parents, in part due to her substance abuse. The daughter has kept a cool distance all these years until she is forced into a situation otherwise. And the parents will eventually learn more about their daughter through the interactions with their daughter's friends and acquaintances. What they learn about her isn't all terrible or painful.
Note here, I haven't mentioned a word about how this piece ends. This is intentional.
Instead, let me say this: at its core, perhaps this is a story about the secrets we keep, and how those secrets inform decisions for which others might not understand, not least the people from whom we've shielded this precious information. Perhaps this is also a story about how the most essential or influential parts of our past lives, however tightly we might attempt to hold or suppress, will always find a way to surface.
Laura van den Berg is the author of the novels Find Me (FSG, 2016) and The Third Hotel (FSG, 2018). She is also the author of two story collections, The Isle of Youth (FSG, 2013) and I Hold a Wolf by the Ears (FSG, 2021).
Review of "Heat Dome" by Kaitlyn Teer, published in Electric Lit
February 8, 2022 April 23, 2022 / Keith Lesmeister / Leave a comment
A gripping and haunting story about parenting, climate change, and community.
I was at first amused by the heat of this story. Right now, I can look out any window of my house, garage, barn, office building, grocery store, and see nothing but snow. True, it is warming up, but the sun here pales in comparison to the unrelenting heat pumped out of this story. What started off as amusement instantly turned to torture (not the story itself — which is great — just the heat. Oh my, the heat!).
The story is told in a collective "we" or first person plural, which is mightily attractive to a person who admires everything he can't do himself. I appreciate this POV on so many levels not least for the inclusive burden of suffering each of these women is having to deal with — for some reason it makes it all the more brutal when the sun is slowly burning away any ounce of sanity held by any of these women. Even so, they're trying: "slicing fruit," "[wiping] the backs of our necks with dishtowels," "[buying] popsicles." All while trying to calm themselves and their families.
"Meteorologists call it a once-in-a-millennia heat wave." This reminds me of when my hometown of Cedar Rapids had something like three "hundred-year floods" in a matter of twenty years. Did I mention I just watched the film "Don't Look Up"? If people don't listen to the science, then maybe a screaming scientist like Jack Dawson or Katniss Everdeen? Maybe Hollywood's the answer, though I have my doubts.
The heat and its effects in "Heat Dome" are simply unrelenting. This story is a crash course in applying pressure to a character or characters until they break and something happens. The only reprieve arrives in beautiful descriptions of the landscape: "…the old two-lane highway down the coast…. curves along sandstone cliffs that slope to the shore." Later, "we descend a trail through red cedar, fir, and madrona." If nature isn't your thing, the narrator offers a more communal answer to the suffering: "We are sweaty, but together."
At least we're sipping wine and dining together, they acknowledge at the end of "Don't Look Up." Never mind the comet. It might not even be real.
Or maybe I shouldn't be so flippant about this communal suffering (at least we're in it together!). The first person plural, after all, is a collection of mothers or mothers-to-be who find solace in these together-moments. The heat and misery of dealing with themselves and their families literally drives them to the ocean for a reprieve. They can't handle it anymore. They have to leave. They lament that this is "their new normal." And since there's not much else to do, besides float in the ocean (and wait for the comet to hit Earth!), they decide to do so with a sense of togetherness. Of "[holding] hands to keep from drifting apart." Because if we're all going to hell, we may as well enter the flames together.
Check out the story here.
Kaitlyn Teer's lyric essays have received prizes from Fourth Genre and Prairie Schooner. Her essay "Drawing A Breath" was a notable for the 2017 Best American Essays anthology and was anthologized in Beautiful Flesh: A Body of Essays (CSU Center for Literary Publishing, 2017). Other work has appeared in Entropy, Redivider, Sweet, Puerto del Sol, and elsewhere. She is a regular contributor to the Ploughshares blog and is at work on a flash collection about parenting and the climate crisis.
Review of "Mouse House" by Amelia Brown, published in Four Way Review
May 27, 2021 May 27, 2021 / Keith Lesmeister / Leave a comment
We meet all relevant characters in the first section: our first-person narrator along with her boyfriend, Eddie, and Eddie's mother (Susan). We're also introduced to a mouse along with the home in which this story takes place. It's Susan's home located in sprawling bucolic Maine where everything is quaint and perfect and people keep tea times (and probably tee times). We're also "two hours north of [the couple's] cluttered apartment in Boston" where they probably don't attend open houses just to see "decorated parlors" and "underground entertainment systems" which is Susan's idea of an ideal afternoon.
The story deftly juxtaposes the narrator's modest upbringing (with the "broken-down Mazda…in the backyard") and Eddie's mother's tea time expectations (not that the two are mutually exclusive). And this alone would be a compelling story full of conflict and compelling situations between the three characters, but the event that propels this piece forward is a game of cat and mouse. Remember that pesky mouse we meet upon arrival from cramped Boston to sprawling Maine? Susan says, "…something has to be done about this mouse." Susan is not keen on keeping company with rodents, but instead of using a traditional mousetrap, the narrator convinces them to use a live-catch trap. The next morning Susan fetches a "box trap" so the narrator won't "feel guilty."
With this goal of catching the mouse, a series of extraordinary—though bizarre—events take place. I won't mention any of them to you. They're just too good to name on this page, and so you'll have to read them for yourself. A small clue: the events in question show in clear detail how out of touch with reality the potential future mother-in-law has become.
This is a fascinating story. I couldn't stop reading.
Amelia Brown's essays and reviews have been published at the Masters Review, CRAFT Literary, Full Stop, and the Ploughshares blog. She lives and writes in Boston.
Review of "Water in the Blood" by Megan Pillow, published in Triquarterly
Mother's Day was over a week ago, but perhaps we ought to do ourselves a favor and read "Water in the Blood" by Megan Pillow, a story, essentially, about everything going to shit—when your world, dreams, husband, and own body fail you, what's bound to happen? This is Laura's story. To say Laura is under a lot of stress would be a sick understatement, and this story is a cautionary tale of what happens to a mother (or parent) under constant barrage from all people and situations in her life.
In grad school, one of my teachers used to talk about stories as nothing more than mounting pressure on a protagonist. Put the protagonist in a vice and keep turning until the character or the vice breaks. I was reminded of this astute writerly advice while reading Pillow's story. Her main character, Laura, is stuck at home, but it's a new home in a new neighborhood where she knows virtually no one, while her husband is literally halfway across the globe in "fucking Antarctica" romping around and writing "beautiful" articles about his adventures. But Laura, we understand, is a better writer: "You would've done better," the husband writes back after Laura reads one of his newly posted articles. Perhaps she's the one who should've penned the article. Perhaps she's the one who should be out galivanting around the arctic ice and writing about her adventures while waiting for shout-outs from adoring fans: "Take me on your next adventure?" writes queenbey9122 to Laura's husband.
Meanwhile, Laura's taking care of three kids and trying not to bleed out. Her last pregnancy and delivery left her with complications spurred on perhaps in part by a condescending male doctor who, of course, knew what was best for her. All the while, as all of this plays out, "There's something in the woods behind the house" and a Florida storm is brewing.
The brilliance of this story is the melding together of all of these mounting pressures. It isn't simply one of these conflicts that'll break our narrator; instead, what Pillow's showing us is what happens to someone who is under constant micro and macro attacks at all times and from those who should be there to help and support (the doctor, the husband), but there's no one to help. Only her and her three needy children, one of whom was born only months ago.
We return now to the original question – what's bound to happen to someone in this situation? When "…she is a great white-hot mass of rage, and she can feel the small dark thing opening its maw, and then she clamps it shut again." What happens when she can't "clamp it shut"? When the protagonist's anguish and frustration are simply too much? Megan Pillow shows us the answer, but you'll have to read the story to find out. Here's a hint: Grab your personal flotation device and maybe an extra oar.
Check out this fantastic, heart-wrenching story here.
Megan Pillow is a graduate of the University of Iowa Writers' Workshop in fiction and holds a Ph.D. in English from the University of Kentucky. Her work has appeared or is forthcoming in, among other places, Electric Literature, SmokeLong Quarterly, Hobart, The Believer, Brevity, and Gay Magazine. Megan has also had stories featured on the Wigleaf Top 50, an essay honored as notable in the 2019 edition of The Best American Essays, and a story honored as distinguished in the 2020 edition of The Best American Short Stories. She lives in Louisville, Kentucky with her two children.


FREE Flash Book-It Game grab the pages as they fly by and put them back into the book. When you book-it you get more points by grabbing the faster pages grab as many pages as you can and book-it. Mouse over a moving page and grab it by left clicking on it and holding it. Then drag it over to the book on the right and drop the page by releasing the mouse button to book-it. free flash book-it game the faster a page is moving the more points it will give so try to grab the fast moving pages. Enjoy playing our free flash book-it game online at The PCman's free games arcade!
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text:
Sarasota Theater
Your independent guide to the best shows in Sarasota
OTHER FAMILY SHOWS IN SARASOTA
The Price Is Right - Live Stage Show
New Shanghai Circus
Disney Princess - The Concert
Dancing With the Stars Event homeBuy ticketsCustomer reviews AnastasiaThe Price Is Right - Live Stage ShowNew Shanghai CircusMasters Of IllusionDisney Princess - The Concert
VAN WEZEL PERFORMING ARTS HALL
Venue home
Pre-theatre dining
Overnight accommodation
Beautiful: The Carole King Musical (Closed Jan 19, 2022)
Bernadette Peters (Jan 23, 2022)
Jersey Boys (Jan 25 - 26, 2022)
Kansas (Jan 28, 2022)
New Shanghai Circus (Jan 29, 2022)
The Choir of Man (Jan 30, 2022)
An American in Paris (Feb 2 - 3, 2022)
Audra McDonald (Feb 11, 2022)
The Simon and Garfunkel Story (Feb 12, 2022)
The Four Phantoms (Feb 14, 2022)
Gladys Knight (Feb 15, 2022)
Paul Anka (Feb 20, 2022)
Celtic Thunder (Feb 23, 2022)
Stayin' Alive (Feb 24, 2022)
Engelbert Humperdinck (Feb 28, 2022)
A Neil Diamond Concert Celebration (Mar 1, 2022)
Menopause - The Musical (Mar 2, 2022)
Celtic Woman (Mar 3, 2022)
Rain - A Tribute to the Beatles (Mar 6, 2022)
Masters Of Illusion (Mar 7, 2022)
Itzhak Perlman (Mar 8, 2022)
The Ten Tenors (Mar 10, 2022)
Chris Botti (Mar 17, 2022)
Anastasia (Mar 18 - 20, 2022)
ABBA: The Concert - A Tribute To ABBA (Mar 27, 2022)
The Price Is Right - Live Stage Show (Mar 29, 2022)
Kenny G. (Apr 5, 2022)
An Officer and a Gentleman (Apr 6 - 7, 2022)
Terry Fator (Apr 10, 2022)
Johnny Mathis (Apr 12, 2022)
South Pacific (Apr 14 - 15, 2022)
Fiddler on the Roof (Apr 19 - 21, 2022)
Il Divo (Apr 22, 2022)
Diana Krall (Apr 23, 2022)
One Night of Queen (May 7, 2022)
Disney Princess - The Concert (Nov 2, 2022)
Van Wezel Performing Arts Hall Please selectVenue homeLocation and directionsPre-theatre diningOvernight accommodationSeating maps Beautiful: The Carole King Musical (Closed Jan 19, 2022)Bernadette Peters (Jan 23, 2022)Jersey Boys (Jan 25 - 26, 2022)Kansas (Jan 28, 2022)New Shanghai Circus (Jan 29, 2022)The Choir of Man (Jan 30, 2022)An American in Paris (Feb 2 - 3, 2022)Audra McDonald (Feb 11, 2022)The Simon and Garfunkel Story (Feb 12, 2022)The Four Phantoms (Feb 14, 2022)Gladys Knight (Feb 15, 2022)Paul Anka (Feb 20, 2022)Celtic Thunder (Feb 23, 2022)Stayin' Alive (Feb 24, 2022)Engelbert Humperdinck (Feb 28, 2022)A Neil Diamond Concert Celebration (Mar 1, 2022)Menopause - The Musical (Mar 2, 2022)Celtic Woman (Mar 3, 2022)Rain - A Tribute to the Beatles (Mar 6, 2022)Masters Of Illusion (Mar 7, 2022)Itzhak Perlman (Mar 8, 2022)The Ten Tenors (Mar 10, 2022)Chris Botti (Mar 17, 2022)Anastasia (Mar 18 - 20, 2022)ABBA: The Concert - A Tribute To ABBA (Mar 27, 2022)The Price Is Right - Live Stage Show (Mar 29, 2022)Kenny G. (Apr 5, 2022)An Officer and a Gentleman (Apr 6 - 7, 2022)Terry Fator (Apr 10, 2022)Johnny Mathis (Apr 12, 2022)South Pacific (Apr 14 - 15, 2022)Fiddler on the Roof (Apr 19 - 21, 2022)Il Divo (Apr 22, 2022)Diana Krall (Apr 23, 2022)One Night of Queen (May 7, 2022)Disney Princess - The Concert (Nov 2, 2022)
777 N Tamiami Trail, Sarasota, FL 34236
Dancing With the Stars Reviews
TV LiveFamily ShowsDance & Ballet
Average customer review: (3.7 Stars)
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Jean martinelli from Madison, Wisconsin
ENTERTAINMENT PLUS
In the past twenty eight years that I have ushered for the Overture Center (and the preceding venue), I have seen many, many shows, including a variety of dance performances and all of the broadway shows. But, nothing prepared me for DWTS. This was part Las Vegas revue, part Magic Mike, part Broadway, part Alvin Ailey and more! The cast was supremely talented and very personable. The dance performances varied from many Latin classics - paso doble anyone? - to hip hop and ballet/modern dance to rock and roll to waltz. The sound track was gorgeous and varied as well, with many of my favorite contemporary music featured. As a result, the audience was absolutely going nuts from beginning to end!!!! This sold-out show left people grinning from ear to ear and dancing and singing out of the theater. I only hope that DWTS will be back next year.
from San Francisco, California
SYTYCD?
Think you can dance's road show hit it big at the Fox Theatre, now called the Bob Hope Theatre, in downtown Stockton. There might have been a few empty seats in the back corners, but the good seats were sold out. The audience was very warm and noisy, and as is the style these days, "whooped" with appreciation instead of applause. The dancers were even better than anticipated from previous appearances on TV. Amazing extensions and elevation. There were no average dancers, all top gypsies! My only complaint was the lighting...the dancers were dimly lighted most of the time, while flashing strobes and LEDs directed at the audience had me closing my eyes in defense. This trendy style of audience insult needs to pass, and quickly. We pay to see what is on the stage, not be blinded by technology. Staging positives? yes, the large screens were able to depict windows and hand painted sets in exquisite detail. When the heavens broke loose with weather and a light show, it was impressive...
Gina Jones from Boston, Massachusetts
FABULOUS SHOW!
Fantastic way to spend a night in Boston. Seats were fab! 1st row behind orchestra seats, so view was awesome. Would totally take my kids and mom! We ate at Abbey Lane directly across from Wang...steps to our seats. Only regret is that Val, Alan, Sasha or Gleb did not pull me up on stage!! Will be at show next year!
D. L. Mullins from Nashville, Tennessee
JUST A LITTLE DISAPPOINTED
I love DWTS and have never missed a single episode in all of it's many seasons on TV. I was especially excited to go see the DWTS Live tour in my hometown of Nashville, TN. Unfortunately, it was pouring rain and there were many long lines waiting to go through security to get into the theatre. Once inside the historic Grand Old Opry House our seats were pretty good in the Mezzanine. I loved seeing all of the Pro dancers up close and personal. The stage is fairly small so it's very different than when you see them perform in the Ballroom on TV with the fancy props, etc. The one real disappointment I had was it was advertised that four celebrity dancers would take part in the Tour this year. I didn't read until after the fact that not "all" would perform in "all cities", but we didn't have one single celebrity here -- not even Bobby Bones who works here or John Schneider. It even stated in the fill-in video that more than the usual one celebrity (the winner) would be on tour.
BTACbill from Birmingham, Alabama
THAT'S ALL THERE IS?
The dancing part lasted about an hour and a half with about 30 minutes of filler. The filler consisted of a couple of videos and Bobby Bones once again confirming that HE CAN'T DANCE. It seemed to me that the cast wanted the show over ASAP so they could get to Huntsville. I felt the same way.
Karen Summers from Houston, Texas
BIG RIPOFF
I paid $300 for 2 tickets just to watch the dance troupe. Not one professional dancer from television or the dozen pros on the face of the tickets were there except for Joe, who emceed the show. BIG HUGE FAT RIPOFF. NEVER AGAIN!!!
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Long-lost painting's rediscovery puts ukiyoe in international spotlight
Mar. 29, 2017	07:00 am JST	 Mar. 29, 2017 | 07:05 am JST
By Alexandra Homma
It's a chilly day for the ladies in Fukagawa, but none of them seems to mind the cold. The 26 courtesans in the painting are preparing for a yet another long day on the job: a lady carries a tray with food, another crouches under a heavy futon (could it be a drunk customer inside?); a beauty retouches her makeup; geishas practice new tunes. An elderly woman, perhaps of a higher rank, leans on the wooden bars observing. The trees are covered in snow — but like everything else in this licensed pleasure district — this too will vanish soon.
The beauties in Snow in Fukagawa, circa 1802-06, are a few of the last Utamaro Kitagawa (1753–1806), Japan's master of bijinga (beauty portraits) and shunga (erotic wood prints), is presumed to have painted in his lifetime. The final installment in Snow, Moon and Flowers, a three-part masterpiece depicting a day at three of the then most popular pleasure areas in Edo (now Tokyo), the painting was last seen in 1948, after which it mysteriously disappeared from the art scene. In March 2014, however, Japan's Okada Museum of Art, startled the world by announcing that it had discovered and reclaimed the work. And now, this miraculous rediscovery not only completes the trio, but it also once again puts ukiyoe in the international spotlight.
Utamaro: The women-expert without a face
By the time Snow in Fukagawa was complete, Utamaro had already earned his reputation as "the man who loved women": a close observant of femininity and courtesans in Japan's most flourishing licensed brothels of the time. Utamaro's works on Edo's women are so profound and so abundant that it would be difficult to think of any other Japanese artist more intent on the opposite sex.
Yet, despite the nearly 2,000 prints he supposedly produced in his lifetime, his life is, to date, veiled in mystery. What we know is that Utamaro was probably born in 1753, possibly in Edo, may have been married and may have had a child; he may have lived in one of Edo's pleasure quarters, or may have had a father who did. His work on Edo's beauties began in the 1780s when he was spotted by a famous publisher at the time as a "brush for hire," or an artist making pictures on demand for a patron. Utamaro's works would gain enormous popularity, establishing him among the most sought-after ukiyoe artists and a specialist in the genre of "beauties." Yet, no letters, diaries or other records that reveal Utamaro's life and personality remain. To the modern art world, Utamaro has no face, nor clear existence.
Snow, Moon, Flowers: Reunited at last
As if to reinforce the mystery surrounding its author, Utamaro's Snow, Moon, Flowers remains one of the most sensational triptych paintings in the history of ukiyoe, if not art itself. The paintings, each published in a different time period and size, represent Edo's licensed brothels as places of ultimate pleasure and leisure. Moon at Shinagawa, circa 1788, depicts an evening at the Shinagawa brothel; Cherry Blossoms at Yoshiwara, circa 1793, presents a spring day of joy under the cherry trees, whereas Snow at Fukagawa, the largest and latest of the three, sees women at work on a cold, Japanese winter day. The three paintings' titles hint of a fleeting moment in one's life: a temporal happiness, satisfaction and pleasure; the darkside of commerce disguised in pretty faces.
Last seen together in 1879, the three paintings are believed to have been brought to France and presented at the Paris World Expo the previous year. The paintings were soon dispersed: Charles Lang Freer, the founder of the Smithsonian's Freer Gallery of Art, acquired Moon at Shinagawa in 1903; Cherry Blossoms at Yoshiwara passed through several hands before entering the collection at the Wadsworth Atheneum Museum of Art in the U.S. in the late 1950s; whereas Snow at Fukagawa returned to Japan in the post WWII period as part of a buyer's private collection. Following two short displays at the famous Matsuzaka department store in the late 1940s, the painting went missing until its discovery by the Okada Museum.
This year, the three paintings will finally be reunited at the same place and time for the first time since the 1880s at the Freer Gallery of Art in Washington D.C. The gallery owns Moon at Shinagawa and — due to its founder Charles Lang Freer's will that no paintings should leave the gallery — is the only place in the world to show all three original pieces together.
In spotlight again: Inventing Utamaro
The reunification of the three paintings and the discovery of Snow has triggered a new ukiyoe interest around the world, largely because the discovery has opened a new Pandora's box for all ukiyoe fans and scholars. The trio's mysterious separation —and discovery—have prompted many to raise more questions about Utamaro and his artistic period, than we already have answered. When exactly did Utamaro make them and for what purpose? Why were two of the paintings preserved in the West, whereas the last one went missing in Japan? And how and when was it discovered? These and more questions are yet to be answered.
Japan and the world were quick to look at Utamaro's works again. Following the rediscovery, the Okada Museum of Art invited the public for an exclusive display of the missing work in 2014, preparing the world for a new Utamaro and ukiyoe fad. In 2015, the Eisei Bunko Museum in Tokyo organized a shunga exhibition, displaying a number of Utamaro's erotic works. The exhibition attracted over 210,000 visitors in three months. This year, the Wadsworth Atheneum Museum of Art in Connecticut, where Cherry Blossoms at Yoshiwara is preserved, presented "Utamaro And The Lure Of Japan", the museum's first exhibit of exclusively Japanese art at the Atheneum since 1951.
And now the largest of them all, the over a century long-anticipated reunion of the trio, is about to take place at the Freer Gallery of Art and Arthur M. Sackler Gallery.
"Inventing Utamaro: A Japanese Masterpiece Rediscovered," which will be on display from April 7 through July 9, though commemorating the reunification of the paintings, is not a retrospective exhibition. It focuses on framing the artworks in the context of three historical moments of "branding and marketing": first, the genius selling of Utamaro's persona as a connoisseur of women; second, the response of art dealers to Japanese "beauty" in Paris and the West in general at the time; and third: the way ukiyoe and Japanese art is perceived in our days. The exhibition places Utamaro in the larger context of 19th century and modern-day Japonisme — the influence of Japanese art on Western art.
But above all, the exhibition provides an opportunity to answer the question we have all secretly wished to ask: what is the significance of snow, moon and flowers in Utamaro's legendary work? As we look into the paintings in search for answers, it all starts to make sense: This historical art is here to stay — even after the snow has melted and the flowers have scattered, the moon will rise and a new day will begin again.
For more information on "Inventing Utamaro: A Japanese Masterpiece Rediscovered," click here.
A special exhibition displaying Snow in Futagawa and Flowers in Yoshiwara, as well as a replica of Moon in Shinagawa, preserved at the Freer Gallery of Art, will be on display at the Okada Museum of Art in Hakone, Japan, from July 28 through October 29, 2017. For more details, click here.
Alfie Noakes
A very interesting article. What a shame that the three original paintings will be reunited in Washington DC and not Japan. Still, it should make for a pleasant trip out to Hakone in summer.
Wakarimasen
I love ukiyoe
nandakandamanda
The article needs to emphasize that these are original paintings and not the woodblock Ukiyoe hanga that we are more accustomed to seeing, which themselves are often three to a triptych.
BertieWooster
It would be great if these pictures could expand to full screen size. They are too tiny to see any detail.


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Q: Prove that $P(\tau<\infty)=1$ and find the distribution of $X_\tau$
Let $\{X_n\}_{n\ge1}$ be a sequence of i.i.d. random variables with distribution $\mu$. For $A\in\mathcal{B}(\mathbb{R}):=\text{Borel $\sigma$-algebra of $\mathbb{R}$}$ with $\mu(A)\in(0,1)$, define
\begin{align*}
\tau=\inf{\{k\ge1, X_k\in A\}}
\end{align*}
(1) Prove that $P(\tau<\infty)=1$.

(2) Prove that $X_\tau$ has distribution given by
\begin{align*}
P(X_\tau\in H)=\frac{\mu(H\cap A)}{\mu(A)},\quad H\in\mathcal{B}(\mathbb{R}).
\end{align*}

I know that $\tau$ is a stopping time with respect to $F_n:=\sigma(X_1,...,X_n)$, in particular $\tau$ is a hitting time but I cannot figure out how to use this information to solve the problem. I feel like this is a pretty standard question and I have overthought myself into frustration with it, any help here would be greatly appreciated.

A: Let $\{X_n\}_{n \in \mathbb N}$ be a family of i.i.d r.vs with distribution $\mu$. Let $A \in \mathcal B(\mathbb R)$ be such that $\mu(A) \in (0,1)$. Define $\tau_A := \inf \{ n \ge 1 : X_n \in A \}$.
a) Note that $\tau_A$ has geometric distribution with parameter $\mu(A)$. Indeed, for $n \ge 1$:
$$ \mathbb P(\tau_A = n) = \mathbb P(X_1,...,X_{n-1} \not \in A, X_n \in A) = \mu(A)(1-\mu(A))^{n-1} $$
So (since $\mu(A) \in (0,1)$ !)
$$ \mathbb P(\tau_A < \infty) = \sum_{n=1}^\infty \mathbb P(\tau_A = n) = \mu(A)\sum_{n=1}^\infty (1-\mu(A))^{n-1} = \frac{\mu(A)}{1-(1-\mu(A))} = 1 $$
b) Let $X_{\tau_A}(\omega) = X_{\tau_A(\omega)}(\omega)$ (it is well defined up to the set of measure $0$)
Let any $H \in \mathcal B(\mathbb R)$. We have:
$$ \mathbb P(X_{\tau_A} \in H) = \sum_{n=1}^\infty \mathbb P(X_n \in H \cap \{ \tau_A = n \}) = \sum_{n=1}^\infty \mathbb P(\{X_1,...,X_{n-1} \not \in A\} \cap  \{X_n \in H \cap A \}) $$
Last equality, during to the fact, that since $\tau_A = n$, we need every $X_1,...,X_{n-1}$ not to fall into $A$, and $X_n$ must fall into $A$ and $H$ simultaneously. Since they are independent, we get it is equal to $(1-\mu(A))^{n-1} \cdot \mu(H \cap A)$, so:
$$ \mathbb P(X_{\tau_A} \in H) = \mu(A\cap H) \sum_{n=1}^\infty (1-\mu(A))^{n-1} = \frac{\mu(A \cap H)}{\mu(A)}$$


text:
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Dawn Chatty: Turkish government has been 'praiseworthy' in approach to Syrian refugee crisis
Professor Dawn Chatty discusses Turkey's response to the Syrian crisis for BBC Viewpoints article
Dawn Chatty: 'Lack of funding' biggest problem for Syrian refugee crisis
Professor Dawn Chatty talks to Al Jazeera about the escalating Syrian refugee crisis
Refuge routes | Naohiko Omata and Josiah Kaplan
Blogs / articles
Dr Naohiko Omata and Dr Josiah Kaplan (Humanitarian Innovation Project) write for Makeshift Magazine on trade and the bustling exchange among different refugee groups in the Nakivale refugee settlement, Uganda
Diletta Lauro wins MSc 2012-13 Best Thesis Prize
We are delighted to announce that this year's Best Thesis Prize has been awarded to Diletta Lauro
In memoriam: Belinda Allan
Belinda Allan, who played an instrumental role in the establishment of the Refugee Studies Centre as its first Development Officer, has died, aged 77. She will be sadly missed
New Asfari bursaries for the International Summer School in Forced Migration
We are pleased to announce a three-year agreement with the Asfari Foundation to attract practitioners working on refugee-related issues from Palestine, Lebanon and Syria to attend the International Summer School on Forced Migration
Za'atari camp: a snapshot of a simmering crisis | Dawn Chatty
Professor Dawn Chatty writes for Debating Development of her experience visiting the Za'atari camp, Jordan
Building a humanitarian solutions database | Louise Bloom
Louise Bloom discusses her role in building a database of innovative ideas that could be applied to humanitarian situations
Refugee livelihoods and private sector engagement in Uganda | Naohiko Omata
Dr Naohiko Omata discusses his recent fieldwork in Kampala, Uganda, as part of the Humanitarian Innovation Project, researching refugee livelihoods and private sector engagement
Innovation, technology and the private sector in refugee protection | Alexander Betts
Dr Alexander Betts introduces the Humanitarian Innovation Project, discussing the role of innovation, technology and the private sector in refugee protection
Development responses to forced migration | Roger Zetter
Emeritus Professor Roger Zetter looks at re-framing humanitarian crises as development opportunities in an address to the 5th Wana Forum 2013
Survival migration and fragile states | Alexander Betts
Dr Alexander Betts outlines his project, 'Survival Migration and Fragile States', exploring new drivers of external displacement which fall outside the dominant legal framework
Forced migration in the Middle East | Dawn Chatty
Professor Dawn Chatty discusses her research as a social anthropologist with a particular focus on forced migration in the Middle East
Governance and administration of justice in refugee camp settings | Kirsten McConnachie
Dr Kirsten McConnachie discusses her research taking a broad comparative approach to refugee self-governance and justice using a mix of criminology, anthropology of law and materials from forced migration studies
Syrian tribes, national politics and the uprising | Dawn Chatty
Professor Dawn Chatty writes for Debating Development on Bedouin tribes and the Syrian uprising
Family ties: remittances and support in Puntland and Somaliland | Laura Hammond
Listen to the 29 May 2013 seminar by Dr Laura Hammond (School of Oriental and African Studies), part of the Trinity term 2013 Public Seminar Series
Call for papers: Refugee Voices
Please note, this call for papers has now closed
Survival migration: failed governance and the crisis of displacement | Alexander Betts
Listen to the 16 October seminar by Dr Alexander Betts (University of Oxford), part of the Michaelmas term 2013 Public Seminar Series
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Listen to the 24 April seminar by Dr Tania Kaiser (School of Oriental and African Studies), part of the Trinity term 2013 Public Seminar Series
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Listen to the 15 May seminar by Dr Toby Kelly (University of Edinburgh), part of the Trinity term 2013 Public Seminar Series
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I had the opportunity to review the IAQG Supply Chain Management Handbook (SCMH). This guideline covers all sorts of topics, including requirements flow-down and change management, sourcing selection and supplier management. A very comprehensive and understandable primer for those who need to get their feet wet and for those experience folks that could use a refresher.


text:
Deep inside the Pelican Nebula a star is in the process of forming as we watch. Credit: Adam Block/Mount Lemmon SkyCenter/University of Arizona
A Pelican births a star with an elephant trunk. No, seriously.
Tag: Nebula
Tag: star birth
My friend Adam Block is an astronomer and astrophotographer at the University of Arizona Mt. Lemmon SkyCenter northeast of Tucson. The skies there are dark, and he commands the Schulman 0.81-meter telescope to probe the skies so he can capture it in monumentally gorgeous images.
I'm always happy when I get an email from him because it means a new image to gawk at. When he sent me one with the link to IC 5070, though, I was momentarily taken aback. What object was that?
Then I saw the picture and realized, ah, the Pelican Nebula! I've seen this myself with a small 'scope and it's funny how much it really does look like a Pelican. But with the 0.81-meter, he has significantly better resolution, and when he sees it it looks like this:
Cooooool. I know this doesn't look like a pelican, but you're only seeing a small piece of it here (I have a wider view below). The Pelican Nebula is about 2,000 light years away or so, easily found in the constellation of Cygnus even with binoculars. It's an interesting object; the most obvious aspect of it is that it's a star-forming gas cloud, with massive stars pummeling the gas around them with ultraviolet light, and the hydrogen responding by glowing characteristically red.
But it's also part of a large molecular cloud: A cold, dense soup of gas and dust that does not glow in visible light, so it can't seen… except in silhouette. At the bottom of the image you can see eerie rolling folds, like lumps of something under a sheet. That's the edge of the molecular cloud, where the thin gas stops and much thicker material takes over. The young, massive, hot, and luminous stars being born in the Pelican slam the molecular cloud with gas and fierce winds of particles as well, eroding it away in a process called photoevaporation, forming those sharp illuminated edges to the darker hummocks.
Stars form in particularly dense knots in the cloud. Some of these knots are so dense they can resist the pummeling from the nascent stellar behemoths, at least for a time. The material around them blows away, leaving long finger-like structures colloquially called "elephant trunks" by astronomers — they're analogous to sandbars in flowing water. Generally, stars form at the tips of the trunks.
You can see one of these just below center and to the right in Adam's image. I gaped at it when I saw it; it's phenomenally long and thin. And then I squinted as I looked at the tip; is that a curved arc of brighter hydrogen gas there?
Yup. I had to chuckle; that was proof positive of a young star at the trunk's tip. Here's a closer view from the NOAO 4-meter Mayall telescope:
Stars inside the Pelican Nebula illuminate and erode away the edge of a dense molecular cloud, creating what's called an ionization front, where stars are being born. Credit: University of Colorado, University of Hawaii and NOAO/AURA/NSF
[Note: Different filters were used for the images, which is why the colors don't match. Adam took the unusual route of using "natural light" filters (red, green, and blue) to make his image instead of narrower filters that select out very specific nebula colors as is usually done.]
See it there, on the right? The star forming itself in the tip is buried in dust and gas, and isn't visible, but its effects are. Young stars form from a disk of material and rotate very rapidly. They also have strong magnetic fields. The fields coil up like vortices, and can take material from the disk and launch it into space in opposite directions. Astronomers call these jets generically, and in this case of a young star we called them Herbig-Haro objects. This one is called HH 555. You see them all over the place inside star-forming nebulae.
So why is this one curved? I found a paper that modeled the jets, and the scientist determined that they are being blown back, either from the expansion of the nebula itself (the gas is hotter than the molecular cloud, so it expands) or from the stellar wind of particles being blown off by a nearby massive star above it.
That was another reason I chuckled when I saw the HH object. Sometimes these jets are curved like propellers due to the star's rotation wobbling over time, but this one was obviously being shaped by a wind of some kind. It's nice to see my first impressions confirmed.
With sufficient imagination, the Pelican Nebula (left) resembles its ornithological namesake (right). The closer images in the article are from the back of the "neck". Credit: Rogelio Bernal Andreo (image)/ Phil Plait (terrible outline)
And this reminds me: The Pelican is located in the constellation of Cygnus (another sky bird), which is up in the summer. Things are warming up around here, and this image is an invitation to take a look myself when the stars align in a few months. I do like to remember that the gorgeous objects I describe here actually exist, and many can be seen without too much trouble.
The occasional reminder of being connected to the sky is always a welcome one.


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High Valley Books
Home › Kai Lung's Golden Hours by Ernest Bramah
Kai Lung's Golden Hours by Ernest Bramah
New York: Doran, 1923. Classic 'oriental style' tale. This is the handsome, colorful original edition. Faint stain on spine label. Some foxing inside. Light rubbing and light sunning.
Ernest Bramah (20 March 1868[1] – 27 June 1942), born Ernest Brammah Smith, was an English author.[2] He published 21 books and numerous short stories and features. His humorous works were ranked with Jerome K Jerome and W.W. Jacobs, his detective stories with Conan Doyle, his politico-science fiction with H.G. Wells and his supernatural stories with Algernon Blackwood. George Orwell acknowledged that Bramah's book, What Might Have Been, influenced his Nineteen Eighty-Four. Bramah created the characters Kai Lung and Max Carrados.
Bramah was a recluse who did not give the public details of his personal life. He died at age 74 in London.
This section does not cite any sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (October 2014)
Ernest Brammah Smith (he later changed his name to Ernest Bramah) dropped out of the Manchester Grammar School at 16, having been close to the bottom of each class in each subject. He went into farming, first as a farm pupil and then in his own right. He was supported by his father who had risen in a short time from a factory hand to a wealthy man. The farming enterprise cost his father £100,000 in today's money. It was while farming that he began to contribute local vignettes to the Birmingham News. Later he wrote a tongue-in-cheek book about his adventure in farming which found few buyers and was remaindered and pulped. After the farming debacle, his father agreed to support him while he made his way in Grub Street. He obtained a position as secretary to Jerome K. Jerome and rose to become editor of one of Jerome's magazines. After leaving Jerome he edited other journals for a publishing firm that later went into bankruptcy.
Bramah attained commercial and critical success with his creation of Kai Lung, an itinerant storyteller. He first appears in The Wallet of Kai Lung which was rejected by eight publishers before Grant Richards published it in 1900. It was still in print a hundred years later. The Kai Lung stories are humorous tales set in China, often with fantasy elements such as dragons and gods.[3]
With Kai Lung, Bramah invented a form of Mandarin English illustrated by the following passages:
Kai Lung rose guardedly to his feet, with many gestures of polite assurance and having bowed several times to indicate his pacific nature, he stood in an attitude of deferential admiration. At this display the elder and less attractive of the maidens fled, uttering loud and continuous cries of apprehension to conceal the direction of her flight.[4]
In particular, there is among this august crowd of Mandarins one Wang Yu, who has departed on three previous occasions without bestowing the reward of a single cash. If the feeble and covetous Wang Yu will place in his very ordinary bowl the price of one of his exceedingly ill-made pipes, this unworthy person will proceed.[5]
After secretly observing the unstudied grace of her movements, the most celebrated picture-maker of the province burned the implements of his craft, and began life anew as a trainer of performing elephants.[6]
The Kai Lung stories are studded with proverbs and aphorisms, such as the following:
"He who lacks a single tael sees many bargains"[7]
"It is a mark of insincerity of purpose to spend one's time in looking for the sacred Emperor in low-class teashops"[8]
"It has been said there are few situations in life that cannot be honourably settled, and without loss of time, either by suicide, a bag of gold or by thrusting a despised antagonist over the edge of a precipice on a dark night"[9]
Bramah also wrote political science fiction. What might Have Been, published in 1907 and republished as The Secret of the League in 1909), is an anti-socialist dystopia reflecting Bramah's conservative political views.[10] It was acknowledged by George Orwell as a source for Nineteen Eighty-Four. Orwell credited it with giving a considerably accurate prediction of the rise of Fascism.[11]
At a time when the English Channel had yet to be crossed by an aeroplane, Bramah foresaw aerial express trains travelling at 10,000 feet, a nationwide wireless-telegraphy network, a proto-fax machine and a cypher typewriter similar to the German Enigma machine.[citation needed]
In 1914, Bramah created Max Carrados, a blind detective. Given the outlandish idea that a blind man could be a detective, in the introduction to the second Carrados book The Eyes of Max Carrados Bramah compared his hero's achievements to those of real life blind people such as Nicholas Saunderson, Lucasian Professor of Mathematics at Cambridge, Blind Jack of Knaresborough the road builder, John Fielding the Bow Street Magistrate of whom it was said he could identify 3,000 thieves by their voices, and Helen Keller.[citation needed]
Bramah has been credited with the invention of the saying, widely quoted as an ancient Chinese curse, "May you live in interesting times", along with "May you come to the attention of those in authority" and "May you find what you are looking for".[12] However, these do not appear in the Kai Lung stories.
Kai Lung books
The Wallet of Kai Lung (1900)
Kai Lung's Golden Hours (1922)
Kai Lung Unrolls His Mat (1928)
The Moon of Much Gladness (1932; published in the USA as The return of Kai Lung)
The Kai Lung Omnibus (1936; includes The Wallet of Kai Lung, Kai Lung's Golden Hours, Kai Lung Unrolls His Mat)
Kai Lung Beneath the Mulberry Tree (1940)
The Celestial Omnibus (1940; selected stories from the earlier books)
Kai Lung: Six (1974)
Kai Lung Raises His Voice (2010; includes Kai Lung: Six, the story from The Specimen Case and four previously unpublished stories)
Guest Bedroom Library Literature
The American Commonwealth by James Bryce
[Elizabeth Taylor] My Elizabeth by Firooz Zahedi
Traveller's Prelude/ Beyond Euphrates Autobiography 1928-1933/ The Coast of Incense Autobiography 1933-1939/ Dust in the Lion's Paw Autobiography 1939-1946
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