Miracle-dz/UniFAR-FTUs huggingface dataset:
A comparison of several methods of macular hole measurement using optical coherence tomography, and their value in predicting anatomical and visual outcomes

Background/Aims To compare several methods of macular hole measurement using optical coherence tomography (OCT), and to assess their predictive capability against anatomical and visual outcomes in a single cohort of patients. Methods A retrospective study of 50 eyes undergoing standardised macular hole surgery. All patients underwent preoperative OCT scanning with measurement of macular hole inner opening diameter, minimum linear diameter, base diameter and macular hole height. Values were calculated for the macular hole index and the tractional hole index. Results Logistic regression analyses indicated that the preoperative base diameter, macular hole inner opening and minimum linear diameter were associated with both anatomical and visual success. Derived parameters as alternatives to these basic ophthalmic parameters add little to the modelling of either anatomical or visual success. Conclusion Base diameter, macular hole inner opening and minimum linear diameter can each be used to predict anatomical and/or functional success in macular hole surgery. Preoperative base diameter is the most useful variable in this regard, as it holds the strongest association with anatomical and visual outcome and is easily measured on a OCT scan.
Calcium antagonists and contractile responses in rat vas deferens and guinea pig ileal smooth muscle.

The effect of depletion of extracellular Ca2+ (Ca2+ext) on the loss of responsiveness of the guinea pig ileal longitudinal muscle (g.p.i.l.m.) and the rat vas deferens (r.v.d.) to K+ and cis-2-methyl-4-dimethylaminomethyl-1,3-dioxolane methiodide (CD), and K+ and noradrenaline (NA), has been examined and compared with the effects of a variety of local anesthetics and calcium antagonists. The results indicate that qualitative similarities are apparent with respect to the dependence of agonist-induced activity on Ca2+ext in both the g.p.i.l. m. and r.v. d. Distinct differences, however, in the Ca2+ translocation processes in these two tissues, in response to the different agonists, can be shown by the use of a variety of 'calcium antagonists' thus indicating that such translocation processes are both tissue and agonist selective. It is thus noted that, contrary to the Ca2+ depletion studies, D 600 and the usually more potent BAY-1040 showed no discrimination of action or potency in their ability to inhibit components of the NA response in the r.v. d. In contrast, D 600 and the more potent BAY-1040 selectively inhibited the tonic component of the K+ response. Treatment with SKF 525A and parethoxycaine (PC) in the g.p.i.l. m. and SKF 525A in the r.v. d. resulted in a nonselective inhibition of responses of the tissues to all stimulants. However, in the r.v. d. PC potentiated NA action, and its methobromide (MeBr) derivative potentiated both NA and K+ action and also, like PC, partially shifted to the left the dose-response curve to Ca2+ in NA-depolarizing Ca-free Tyrode's. The quaternary MeBr and the tertiary 2-chloroethyl (2Cl) derivatives of SKF 525A and PC were selectively more effective against CD- than K+ supported contractile activity in the g.p.i.l. m. and the 2Cl derivatives were more effective against NA than K+ responses in the r.v. d. The 2Cl derivative of PC also was more effective in antagonizing the Ca2+ dose-response curve in high-CD or high-NA than in high-K+ Ca2+-free Tyrode's.
Novel Anonymous Key Establishment Protocol for Isolated Smart Meters

In a smart grid, fine-grained usage reports of consumers are gathered using some computationally constrained smart measurement devices. One of the most challenging requirements in the data aggregation is how to securely read the consumption data, while putting the least possible overhead on smart meters. For this reason, recently, two efficient security protocols have been proposed to be used for subsequent secure consumption reports gathered from isolated smart measurement devices. Nonetheless, in both protocols, for each key establishment, the smart reader requires to connect to the electricity service provider (ESP) via the Internet. This paper proposes a novel key establishment protocol, which is free from the ESP involvement during the key agreement and benefits from notable reduction in the communication cost. Our thorough efficiency and security analyses indicate the eminence of the proposed security protocol.
Developmental basis for filamin-A-associated myxomatous mitral valve disease.

AIMS We hypothesized that the structure and function of the mature valves is largely dependent upon how these tissues are built during development, and defects in how the valves are built can lead to the pathological progression of a disease phenotype. Thus, we sought to uncover potential developmental origins and mechanistic underpinnings causal to myxomatous mitral valve disease. We focus on how filamin-A, a cytoskeletal binding protein with strong links to human myxomatous valve disease, can function as a regulatory interface to control proper mitral valve development. METHODS AND RESULTS Filamin-A-deficient mice exhibit abnormally enlarged mitral valves during foetal life, which progresses to a myxomatous phenotype by 2 months of age. Through expression studies, in silico modelling, 3D morphometry, biochemical studies, and 3D matrix assays, we demonstrate that the inception of the valve disease occurs during foetal life and can be attributed, in part, to a deficiency of interstitial cells to efficiently organize the extracellular matrix (ECM). This ECM organization during foetal valve gestation is due, in part, to molecular interactions between filamin-A, serotonin, and the cross-linking enzyme, transglutaminase-2 (TG2). Pharmacological and genetic perturbations that inhibit serotonin-TG2-filamin-A interactions lead to impaired ECM remodelling and engender progression to a myxomatous valve phenotype. CONCLUSIONS These findings illustrate a molecular mechanism by which valve interstitial cells, through a serotonin, TG, and filamin-A pathway, regulate matrix organization during foetal valve development. Additionally, these data indicate that disrupting key regulatory interactions during valve development can set the stage for the generation of postnatal myxomatous valve disease.
Interest Rate Determination in China: Past, Present, and Future

How should we think about the determination of interest rates in China after interest rate liberalization? Would effective deposit rates, lending rates, and bond yields move higher or lower? We argue that interest rates in a liberalized environment would need to be anchored by monetary policy. To achieve price and output (or employment) stabilization, the policy rate should be set close to China’s equilibrium or natural rate. We sketch three preliminary approaches to estimation of the natural rate. Based on this analysis, we argue that interest rates on large deposits and short-term money-market rates would likely move higher following liberalization. The effect on effective lending rates is somewhat ambiguous, as the contestability of the banking sector and the competition from the bond markets are likely to increase. We leave the determination of the curvature of the yield curve to future research.
Meta‐analysis indicates that oxidative stress is both a constraint on and a cost of growth

Abstract Oxidative stress (OS) as a proximate mechanism for life‐history trade‐offs is widespread in the literature. One such resource allocation trade‐off involves growth rate, and theory suggests that OS might act as both a constraint on and a cost of growth, yet studies investigating this have produced conflicting results. Here, we use meta‐analysis to investigate whether increased OS levels impact on growth (OS as a constraint on growth) and whether greater growth rates can increase OS (OS as a cost of growth). The role of OS as a constraint on growth was supported by the meta‐analysis. Greater OS, in terms of either increased damage or reduced levels of antioxidants, was associated with reduced growth although the effect depended on the experimental manipulation used. Our results also support an oxidative cost of growth, at least in terms of increased oxidative damage, although faster growth was not associated with a change in antioxidant levels. These findings that OS can act as a constraint on growth support theoretical links between OS and animal life histories and provide evidence for a growth–self‐maintenance trade‐off. Furthermore, the apparent oxidative costs of growth imply individuals cannot alter this trade‐off when faced with enhanced growth. We offer a starting platform for future research and recommend the use of oxidative damage biomarkers in nonlethal tissue to investigate the growth–OS relationship further.
TNF-αneutralization ameliorates the severity of murine Crohn's-like ileitis by abrogation of intestinal epithelial cell apoptosis

Tumor necrosis factor α (TNF-α) is an important mediator of programmed cell death, and TNF-α blockade significantly improves disease severity in several inflammatory conditions, including Crohn's disease (CD), one of the idiopathic inflammatory bowel diseases. However, the precise mechanism(s) of action of anti-TNF-α therapy in CD remains poorly understood. SAMP1/YitFc mice develop a spontaneous ileitis with similarities to human CD in regard to histological features as well as response to conventional treatments. In this report, we tested the novel hypothesis that the beneficial effects of anti-TNF-α therapy in CD are mediated by a mechanism that involves down-regulation of intestinal epithelial cell (IEC) apoptosis. Similar to the efficacy of monoclonal anti-TNF-α antibodies in human CD, a single injection of a chimeric anti-murine TNF-α antibody into SAMP1/YitFc mice resulted in a marked suppression of intestinal inflammation and epithelial cell damage compared with mice injected with an isotype control antibody. These effects were associated with a significant reduction in apoptosis of freshly isolated IEC as assessed by propidium iodide staining and DNA laddering. In contrast, an increase in lamina propria mononuclear cell apoptosis was observed in anti-TNF-α-treated mice compared with control. These results were confirmed in vivo by using the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling-assay. In addition, neutralization of TNF-α reduced membrane bound FAS/CD95 expression in IEC from SAMP1/YitFc mice compared with control antibody. These data demonstrate a novel mechanism of action of anti-TNF-α therapy that involves homeostatic regulation of mucosal cell apoptosis, which results in the net decrease of chronic inflammation typically found in CD.
The effect of the sagittal ridge angle on cartilage stress in the equine metacarpo-phalangeal (fetlock) joint

Abstract Fatigue failure of bones of the metacarpo-phalangeal (fetlock, MCP) joint is common in thoroughbred racehorses. Stresses within the fetlock joint cartilages are affected by the morphology of the third metacarpal bone (MC3) and proximal phalangeal bone, and the steepness of the median sagittal ridge of MC3 is believed to be associated with fracture. This study investigated the influence of the steepness of the sagittal ridge on cartilage stress distribution using a finite element model of the joint. Changes to the steepness of the sagittal ridge were made by applying a parabolic function to the mesh, creating four different models with sagittal ridge angles ranging from 95° to 105°. In the fetlock joint of Thoroughbred racehorses, sagittal ridge angles of >100° were associated with higher Von Mises stresses in cartilage at the palmar aspect of the condylar groove than such stresses in joints with sagittal ridge angles of <100°. Stresses were high in the specific region where fractures are known to originate in MC3. This aspect of morphology of the fetlock joint thus appears to play an important role in the magnitude and distribution of cartilage stresses, which, when acting on the underlying hard tissues of the articular calcified cartilage and subchondral bone may play a role in the initiation of fatigue fracture in the third metacarpal bone.
Evolution toward Fit

This paper uses a longitudinal case study of the mutual fund provider, The Vanguard Group, to understand the developmental processes that lead to organizational configurations and fit. A new method for determining an organization's core elements is developed, and four processes are identified that describe the creation and subsequent elaboration of these core elements: thickening (reinforcement of an existing core element by new elaborating elements), patching (creation of a new core element and its reinforcement by new elaborating elements), coasting (no further elaboration of a new core element in a given period), and trimming (deletion of a core element and its elaborating elements). The four processes are used to describe organizations' development paths toward configurations and their transitions between configurations, including two new ideal types, termed thin-to-thick and patch-by-patch, as well as two known paths between configurations, the punctuated equilibrium path and reorientation through linear progression.
Topics in portfolio optimisation and systemic risk

This thesis is concerned with different sources of risk occurring in financial markets. We follow a bottom-up approach by carrying out an analysis from the perspective of a single investor to the whole banking system. We first consider an investor who faces parameter uncertainty in a continuous-time financial market. We model the investor’s preference by a power utility function leading to constant relative risk aversion. We show that the loss in expected utility is large when using a simple plug-in strategy for unknown parameters. We also provide theoretical results that show the tradeoff between holding a well-diversified portfolio and a portfolio that is robust against estimation errors. To reduce the effect of estimation, we constrain the weights of the risky assets with a norm leading to a sparse portfolio. We provide analytical results that show how the sparsity of the constrained portfolio depends on the coefficient of relative risk aversion. Based on a simulation study, we demonstrate the existence and the uniqueness of an optimal bound on the norm for each level of relative risk aversion. Next, we consider the interbank lending market as a network in which the nodes represent banks and the directed edges represent interbank liabilities. The interbank network is characterised by the matrix of liabilities whose entries are not directly observable, as bank balance sheets provide only total exposures to the interbank market. Using a Bayesian approach, we assume that each entry follows a Gamma distributed prior. We then construct a Gibbs sampler of the conditional joint distribution of interbank liabilities given total interbank liabilities and total interbank assets. We illustrate our methodology with a stress test on two networks of eleven and seventysix banks. We identify under which circumstances the choice of the prior influences the stability and the structure of the network.
Deep learning of the splicing (epi)genetic code reveals a novel candidate mechanism linking histone modifications to ESC fate decision

Alternative splicing (AS) is a genetically and epigenetically regulated pre-mRNA processing to increase transcriptome and proteome diversity. Comprehensively decoding these regulatory mechanisms holds promise in getting deeper insights into a variety of biological contexts involving in AS, such as development and diseases. We assembled splicing (epi)genetic code, DeepCode, for human embryonic stem cell (hESC) differentiation by integrating heterogeneous features of genomic sequences, 16 histone modifications with a multi-label deep neural network. With the advantages of epigenetic features, DeepCode significantly improves the performance in predicting the splicing patterns and their changes during hESC differentiation. Meanwhile, DeepCode reveals the superiority of epigenomic features and their dominant roles in decoding AS patterns, highlighting the necessity of including the epigenetic properties when assembling a more comprehensive splicing code. Moreover, DeepCode allows the robust predictions across cell lineages and datasets. Especially, we identified a putative H3K36me3-regulated AS event leading to a nonsense-mediated mRNA decay of BARD1. Reduced BARD1 expression results in the attenuation of ATM/ATR signalling activities and further the hESC differentiation. These results suggest a novel candidate mechanism linking histone modifications to hESC fate decision. In addition, when trained in different contexts, DeepCode can be expanded to a variety of biological and biomedical fields.
Estimating Density Dependence from Population Time Series Using Demographic Theory and Life‐History Data

For populations with a density‐dependent life history reproducing at discrete annual intervals, we analyze small or moderate fluctuations in population size around a stable equilibrium, which is applicable to many vertebrate populations. Using a life history having age at maturity α, with stochasticity and density dependence in adult recruitment and mortality, we derive a linearized autoregressive equation with time lags from 1 to α yr. Contrary to current interpretations, the coefficients corresponding to different time lags in the autoregressive dynamics are not simply measures of delayed density dependence but also depend on life‐history parameters. The theory indicates that the total density dependence in a life history, D, should be defined as the negative elasticity of population growth rate per generation with respect to change in population size, \documentclass{aastex} \usepackage{amsbsy} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{bm} \usepackage{mathrsfs} \usepackage{pifont} \usepackage{stmaryrd} \usepackage{textcomp} \usepackage{portland,xspace} \usepackage{amsmath,amsxtra} \usepackage[OT2,OT1]{fontenc} \newcommand\cyr{ \renewcommand\rmdefault{wncyr} \renewcommand\sfdefault{wncyss} \renewcommand\encodingdefault{OT2} \normalfont \selectfont} \DeclareTextFontCommand{\textcyr}{\cyr} \pagestyle{empty} \DeclareMathSizes{10}{9}{7}{6} \begin{document} \landscape $$D=-\partial \mathrm{ln}\,\lambda ^{T}/ \partial \mathrm{ln}\,N$$ \end{document} , where λ is the asymptotic multiplicative growth rate per year, T is the generation time, and N is adult population size. The total density dependence in the life history, D, can be estimated from the sum of the autoregression coefficients. We estimate D in populations of seven vertebrate species for which life‐history studies and unusually long time series of complete population censuses are available. Estimates of D were statistically significant and large, on the order of 1 or higher, indicating strong density dependence in five of the seven species. We also show that life history can explain the qualitative features of population autocorrelation functions and power spectra and observations of increasing empirical variance in population size with increasing length of time series.
Carcinogenic Potential of Ovulatory Genotoxicity1

Abstract Ovulation is a rate-limiting event for the perpetuation of a species; unfortunately, it imparts a cancer risk. Reactive oxidants generated during the mechanics of ovulatory follicular rupture damage the DNA of ovarian surface epithelial cells that are located within a limited diffusion radius. Those cells that survive the trauma of ovulation, along the margins of a ruptured follicle, proliferate and migrate to reconcile the discontinuity within the ovarian epithelium created at the site of oocyte release. It is conceivable that clonal expansion of an ovarian surface epithelial cell with unrepaired DNA, but not committed to death, could be an initiating factor in the etiology of common ovarian cancer. In fact, the majority of cancers of the ovary are derived from the surface epithelium; and circumstances that avert ovulation (oral contraceptive use, pregnancy/lactation) protect against ovarian adenocarcinoma. Not surprisingly, the genotoxic potential of ovulation is exacerbated by malfunctions in tumor suppressor/cell-cycle arrest and base-excision repair mechanisms. Recent experimental evidence indicates that vitamin E and progesterone protect against ovarian metaplasia by negating the oxidative stress of ovulation and by enhancing the repair capacity (genomic integrity) of the surface epithelium, respectively. Ovarian cancer of surface epithelial origin is a deadly insidious disease because it characteristically remains asymptomatic until it has metastasized throughout the abdominal cavity; therefore, prevention is a high priority.
Keeping Vulnerable Children Safe from Pertussis Preventing Nosocomial Pertussis Transmission in the Neonatal Intensive Care Unit

Objective. To examine the impact of different acellular pertussis booster vaccination strategies on the probability of a nosocomial pertussis outbreak occurring and the distribution of outbreak sizes observed for each intervention strategy. Setting. Neonatal intensive care unit. Methods. We developed a stochastic, agent-based simulation model to examine the impact of booster vaccination strategies for pertussis on health care-related transmission. Results. Our results demonstrate that healthcare worker booster vaccination decreases the probability of secondary transmission from 49% (base case, no boosting) to 2% (if 95% of healthcare workers are boosted) and decreases final outbreak size. Boosting family caregivers did not have a clinically significant impact on nosocomial disease transmission. Conclusion. The provision of booster vaccine to healthcare workers in the neonatal intensive care unit substantially reduces the risk of hospital-centered pertussis outbreaks in a manner that enhances the health of hospitalized children. A formal health economic analysis of this finding is currently under way. Policies to protect patient safety in pediatric facilities should include compliance with the United States Advisory Committee on Immunization Practices, which recommends provision of pertussis booster vaccination to healthcare workers.
Testing Forward Rate Unbiasedness in India: An Econometric Analysis of Indo - Us Forex Market

The 'Unbiased Forward Rate Hypothesis' (UFH) states that the forward exchange rate of any foreign currency must be an unbiased predictor of the future spot rate. In developed economies, considerable empirical work has been undertaken by researchers to test the validity of UFH; however the results have been quite mixed. In the Indian context, little empirical (or even theoretical) work has been undertaken to test/examine/investigate the validity of UFH in the Indian forex market. In this paper, we attempt to reexamine in Indian context the familiar relationship between forward and future spot rate. Using the rates for the US Dollar on a monthly basis, we use 'level' specification to test for UFH in the Indo - US foreign exchange rate market. Cointegration tests are performed to confirm the legitimacy of forward rate and spot rate being included in regression. Evidence of serial correlation is found and models for correction of serial correlation are used. The data, taken from the Reserve Bank of India, covers a period from September 2000 to January 2007. Our investigations reveal that the Indian forex market does not fully support the UFH. For the entire sample period, the evidences indicate that even though the current forward rate has a significant impact in predicting the future spot rate, however, enough variability remain to make the predictions a suspect. Based on our evidences, we highlight some reasons as to why the UHF fails in the Indian forex market and suggest areas for further research.