Context-Preserving Two-Stage Video Domain Translation for Portrait Stylization

Portrait stylization, which translates a real human face image into an artistically stylized image, has attracted considerable interest and many prior works have shown impressive quality in recent years. However, despite their remarkable performances in the image-level translation tasks, prior methods show unsatisfactory results when they are applied to the video domain. To address the issue, we propose a novel two-stage video translation framework with an objective function which enforces a model to generate a temporally coherent stylized video while preserving context in the source video. Furthermore, our model runs in real-time with the latency of 0.011 seconds per frame and requires only 5.6M parameters, and thus is widely applicable to practical real-world applications.Comment: 5 pages, 3 figures, CVPR 2023 Workshop on AI for Content Creatio

Loss of IQSEC3 Disrupts GABAergic Synapse Maintenance and Decreases Somatostatin Expression in the Hippocampus

Gephyrin interacts with various GABAergic synaptic proteins to organize GABAergic synapse development. Among the multitude of gephyrin-binding proteins is IQSEC3, a recently identified component at GABAergic synapses that acts through its ADP ribosylation factor-guanine nucleotide exchange factor (ARF-GEF) activity to orchestrate GABAergic synapse formation. Here, we show that IQSEC3 knockdown (KD) reduced GABAergic synaptic density in vivo, suggesting that IQSEC3 is required for GABAergic synapse maintenance in vivo. We further show that IQSEC3 KD in the dentate gyrus (DG) increases seizure susceptibility and triggers selective depletion of somatostatin (SST) peptides in the DG hilus in an ARF-GEP activity-dependent manner. Strikingly, selective introduction of SST into SST interneurons in DG-specific IQSEC3-KD mice reverses GABAergic synaptic deficits. Thus, our data suggest that IQSEC3 is required for linking gephyrin-GABAA receptor complexes with ARF-dependent pathways to prevent aberrant, runaway excitation and thereby contributes to the integrity of SST interneurons and proper GABAergic synapse maintenance. © 2020 The Author(s) In this study, Kim et al. investigate the effect of loss of function of IQSEC3, a gephyrin-binding GABAergic synapse-specific ARF-GEF, using hippocampal dentate gyrus (DG)-specific IQSEC3-knockdown (KD) mice. Strikingly, IQSEC3 KD causes a massive reduction of somatostatin (SST) expression. The restricted SST expression in SST+ interneurons reverses the pathological phenotypes. © 2020 The Author(s)1

Npas4 regulates IQSEC3 expression in hippocampal somatostatin interneurons to mediate anxiety-like behavior

Activity-dependent GABAergic synapse plasticity is important for normal brain functions, but the underlying molecular mechanisms remain incompletely understood. Here, we show that Npas4 (neuronal PAS-domain protein 4) transcriptionally regulates the expression of IQSEC3, a GABAergic synapse-specific guanine nucleotide-exchange factor for ADP-ribosylation factor (ARF-GEF) that directly interacts with gephyrin. Neuronal activation by an enriched environment induces Npas4-mediated upregulation of IQSEC3 protein specifically in CA1 stratum oriens layer somatostatin (SST)-expressing GABAergic interneurons. SST+ interneuron-specific knockout (KO) of Npas4 compromises synaptic transmission in these GABAergic interneurons, increases neuronal activity in CA1 pyramidal neurons, and reduces anxiety behavior, all of which are normalized by the expression of wild-type IQSEC3, but not a dominant-negative ARF-GEF-inactive mutant, in SST+ interneurons of Npas4-KO mice. Our results suggest that IQSEC3 is a key GABAergic synapse component that is directed by Npas4 and ARF activity, specifically in SST+ interneurons, to orchestrate excitation-to-inhibition balance and control anxiety-like behavior.1

Risk factors in nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease, with a global prevalence estimated at approximately 25%. NAFLD is also the leading cause of liver cirrhosis, hepatocellular carcinoma, and death. Additionally, the risk of cardiovascular disease increases with greater NAFLD severity. The liver- and cardiovascular disease-related mortality incident rate ratios among the NAFLD population were 0.77 and 4.79 per 1,000 person-years, respectively. We intend to discuss the risk factors associated with NAFLD in terms of development and progression. Obesity or higher body mass index is closely associated with NAFLD in a dose-dependent manner, but growing evidence suggests that central obesity plays a more important role in the development of NAFLD. Saturated fat and fructose have been reported to be closely related to NAFLD. Fructose intake promotes lipogenesis and impairs mitochondria fat oxidation. The presence of type 2 diabetes is the most powerful predictive risk factor for hepatic fibrosis in patients with NAFLD. Single nucleotide polymorphism is not only associated with the prevalence of NAFLD but also associated with increased liver disease mortality. Obstructive sleep apnea, intestinal dysbiosis, and sarcopenia are associated with the development of NAFL

Development of a campus-based intervention program to strengthen food literacy among university students: A qualitative formative study

Objectives: This study aimed to develop a campus-based intervention program to enhance food literacy (FL) among university students. Methods: In the initial phase, we conducted a literature review of FL intervention studies and held in-depth interviews with university students to identify facilitators and barriers to improving and practicing FL. Expert counseling sessions were conducted with nutrition education, marketing, and service design professionals. The results of this phase led to the creation of an initial curriculum draft. In the second phase, a follow-up survey was conducted with young adults to assess the acceptability of the developed curriculum. After the follow-up survey, additional meetings were conducted with the aforementioned experts, and the curriculum was further refined based on their input. Results: An 11-week FL intervention program was devised using constructs from the Social Cognitive Theory. The weekly curriculum consisted of 90-min theory-based and 90-min hands-on experience sessions. Three primary aspects of FL were covered: nutrition and food safety, cultural and relational dimensions, and socio-ecological aspects. Program highlights included cooking sessions for crafting traditional Korean desserts, lectures on animal welfare, insights into zero-waste practices, and communal eating experiences. Based on the study team’s previous research, the program also addressed mindful eating, helping participants understand the relationship with their eating habits, and providing strategies to manage negative emotions without resorting to food. Yoga sessions and local farm visits were incorporated into the curriculum to promote holistic well-being. Conclusions: This study elucidated the comprehensive process of creating a campus-based curriculum to enhance FL among university students, a group particularly susceptible to problematic eating behaviors and low FL levels. The developed program can serve as a blueprint for adaptation to other campuses seeking to bolster students’ FL

Different effects of prolonged β-adrenergic stimulation on heart and cerebral artery

The aim of this review was to understand the effects of β-adrenergic stimulation on oxidative stress, structural remodeling, and functional alterations in the heart and cerebral artery. Diverse stimuli activate the sympathetic nervous system, leading to increased levels of catecholamines. Long-term overstimulation of the β-adrenergic receptor (βAR) in response to catecholamines causes cardiovascular diseases, including cardiac hypertrophy, stroke, coronary artery disease, and heart failure. Although catecholamines have identical sites of action in the heart and cerebral artery, the structural and functional modifications differentially activate intracellular signaling cascades. βAR-stimulation can increase oxidative stress in the heart and cerebral artery, but has also been shown to induce different cytoskeletal and functional modifications by modulating various components of the βAR signal transduction pathways. Stimulation of βAR leads to cardiac dysfunction due to an overload of intracellular Ca2+ in cardiomyocytes. However, this stimulation induces vascular dysfunction through disruption of actin cytoskeleton in vascular smooth muscle cells. Many studies have shown that excessive concentrations of catecholamines during stressful conditions can produce coronary spasms or arrhythmias by inducing Ca2+-handling abnormalities and impairing energy production in mitochondria, In this article, we highlight the different fates caused by excessive oxidative stress and disruptions in the cytoskeletal proteome network in the heart and the cerebral artery in responsed to prolonged βAR-stimulation

Association of a dysbiotic oral microbiota with the development of focal lymphocytic sialadenitis in I kappa B-zeta-deficient mice

Mice lacking I kappa B-zeta, a protein encoded by the Nfkbiz gene, spontaneously develop a Sjogren's syndrome-like disease involving the lachrymal glands, but no salivary gland symptoms have been reported. We found that Nfkbiz(-/-) female mice presented a significantly reduced salivary flow rate, focal lymphocytic sialadenitis (FLS), and a dysbiotic oral microbiota at week 24. To dissect the contributions of genetic and environmental factors to the salivary gland phenotype, Nfkbiz(+/+) and Nfkbiz(-/-) mice were cohoused after weaning and evaluated at week 20. Cohousing alleviated the salivary gland phenotype of Nfkbiz(-/-) mice but did not induce any disease phenotype in Nfkbiz(+/+) mice. Additionally, the oral microbiota in the cohoused mice was synchronized toward that in Nfkbiz(+/+) mice. In conclusion, I kappa B-zeta-deficient mice developed hyposalivation and FLS, in which a dysbiotic oral microbiota played an important role. This finding suggests that the dysbiotic oral microbiota could be a therapeutic target.Y