SDFE-LV: A Large-Scale, Multi-Source, and Unconstrained Database for Spotting Dynamic Facial Expressions in Long Videos

In this paper, we present a large-scale, multi-source, and unconstrained database called SDFE-LV for spotting the onset and offset frames of a complete dynamic facial expression from long videos, which is known as the topic of dynamic facial expression spotting (DFES) and a vital prior step for lots of facial expression analysis tasks. Specifically, SDFE-LV consists of 1,191 long videos, each of which contains one or more complete dynamic facial expressions. Moreover, each complete dynamic facial expression in its corresponding long video was independently labeled for five times by 10 well-trained annotators. To the best of our knowledge, SDFE-LV is the first unconstrained large-scale database for the DFES task whose long videos are collected from multiple real-world/closely real-world media sources, e.g., TV interviews, documentaries, movies, and we-media short videos. Therefore, DFES tasks on SDFE-LV database will encounter numerous difficulties in practice such as head posture changes, occlusions, and illumination. We also provided a comprehensive benchmark evaluation from different angles by using lots of recent state-of-the-art deep spotting methods and hence researchers interested in DFES can quickly and easily get started. Finally, with the deep discussions on the experimental evaluation results, we attempt to point out several meaningful directions to deal with DFES tasks and hope that DFES can be better advanced in the future. In addition, SDFE-LV will be freely released for academic use only as soon as possible

Development and application of the Chinese version of the adult strabismus quality of life questionnaire (AS-20): a cross-sectional study

Abstract Background Patients with strabismus experience visual dysfunction, self-image disorders, low self-esteem, and social and emotional barriers, which adversely influence their health-related quality of life (HRQoL). Currently no strabismus-specific questionnaire is available in China to identify patients’ quality of life and to evaluate the effectiveness of strabismus treatment. The aims of the present study were to validate the Chinese-language version of the Adult Strabismus Quality of Life Questionnaire (AS-20) and to evaluate the impacts of strabismus on the quality of life among Chinese strabismus patients. Methods Two hundred and fifty-five Chinese adults with strabismus, one hundred visually normal adults and one hundred patients with other eye diseases completed the Chinese version of AS-20. Psychometric properties of the Chinese AS-20 were examined by Cronbach’s α coefficient, test-retest and split-half reliability, and construct and criterion-related validity. Independent-samples t test and one-way ANOVA analyses were conducted to explore the impact of demographic factors and clinical characteristics on HRQoL in Chinese strabismic adults. Results The final AS-20 in Chinese (AS-C) included 18 items and two subscales: psychosocial (12 items) and function (6 items). The Cronbach’s α was 0.908 for overall scale, with 0.913 and 0.808 for \u27psychosocial’ and \u27function’ subscales respectively, indicating high internal consistency reliability. The mean of the overall AS-C score among strabismus patients was 62.80 ± 18.94, significantly lower than that in visually normal adults (t = -18.693, P \u3c 0.001), and in patients with other eye diseases (t = -5.512, P \u3c 0.001). Conclusions The AS-C is a culturally appropriate tool to evaluate the HRQoL in Chinese strabismus adults. The psychosocial health well-being and overall quality of life in strabismic patients should receive greater emphasis

Relativistic hyperpolarizabilities for atomic H, Li, and Be+^+ systems

The hyperpolarizability of an atom is a property that describes the nonlinear interaction between an atom and an external electric field leading to a higher-order Stark shift. Accurate evaluations of these coefficients for various systems are crucial to improve experimental precision in advanced atom-based clocks. However, there is a dearth of reports on atomic hyperpolarizabilities, particularly regarding relativistic hyperpolarizabilities. Thus, in this paper, we use fourth-order perturbation theory to establish a universal formula for the hyperpolarizability and calculate the relativistic hyperpolarizabilities of low-lying states for the monovalent electronic atomic systems H, Li, and Be$^+$. The highly accurate results given here for the H atom could serve as benchmarks for other theoretical methods.Comment: 12 pages; 1 figur

Puerarin attenuates pressure overload-induced cardiac hypertrophy

AbstractBackgroundPuerarin is the most abundant isoflavonoid in kudzu root. It has been used to treat angina pectoris and myocardial infarction clinically. However, little is known about the effect of puerarin on cardiac hypertrophy.MethodsAortic banding (AB) was performed to induce cardiac hypertrophy in mice. Puerarin premixed in diets was administered to mice after one week of AB. Echocardiography and catheter-based measurements of hemodynamic parameters were performed at 7 weeks after starting puerarin treatment (8 weeks post-surgery). The extent of cardiac hypertrophy was also evaluated by pathological and molecular analyses of heart samples. Cardiomyocyte apoptosis was assessed by measuring Bax and Bcl-2 protein expression and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. In addition, the inhibitory effect of puerarin (1μM, 5μM, 10μM, 20μM, 40μM) on mRNA expression of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in Ang II (1μM)-stimulated H9c2 cells was investigated using quantitative real-time reverse transcription-polymerase chain reaction.ResultsEchocardiography and catheter-based measurements of hemodynamic parameters at 7 weeks revealed the amelioration of systolic and diastolic abnormalities. Puerarin also decreased cardiac fibrosis in AB mice. Moreover, the beneficial effect of puerarin was associated with the normalization in gene expression of hypertrophic and fibrotic markers. Further studies showed that pressure overload significantly induced the activation of phosphoinositide 3-kinase (PI3K)/Akt signaling and c-Jun N-terminal kinase (JNK) signaling, which was blocked by puerarin treatment. Cardiomyocyte apoptosis and induction of Bax in response to AB were suppressed by puerarin. Furthermore, the increased mRNA expression of ANP and BNP induced by Ang II (1μM) was restrained to a different extent by different concentrations of puerarin.ConclusionPuerarin may have an ability to retard the progression of cardiac hypertrophy and apoptosis which is probably mediated by the blockade of PI3K/Akt and JNK signaling pathways

Activating Transcription Factor 3 Deficiency Promotes Cardiac Hypertrophy, Dysfunction, and Fibrosis Induced by Pressure Overload

Activating transcription factor 3 (ATF3), which is encoded by an adaptive-response gene induced by various stimuli, plays an important role in the cardiovascular system. However, the effect of ATF3 on cardiac hypertrophy induced by a pathological stimulus has not been determined. Here, we investigated the effects of ATF3 deficiency on cardiac hypertrophy using in vitro and in vivo models. Aortic banding (AB) was performed to induce cardiac hypertrophy in mice. Cardiac hypertrophy was estimated by echocardiographic and hemodynamic measurements and by pathological and molecular analysis. ATF3 deficiency promoted cardiac hypertrophy, dysfunction and fibrosis after 4 weeks of AB compared to the wild type (WT) mice. Furthermore, enhanced activation of the MEK-ERK1/2 and JNK pathways was found in ATF3-knockout (KO) mice compared to WT mice. In vitro studies performed in cultured neonatal mouse cardiomyocytes confirmed that ATF3 deficiency promotes cardiomyocyte hypertrophy induced by angiotensin II, which was associated with the amplification of MEK-ERK1/2 and JNK signaling. Our results suggested that ATF3 plays a crucial role in the development of cardiac hypertrophy via negative regulation of the MEK-ERK1/2 and JNK pathways