Breathing Life into Faces: Speech-driven 3D Facial Animation with Natural Head Pose and Detailed Shape

The creation of lifelike speech-driven 3D facial animation requires a natural and precise synchronization between audio input and facial expressions. However, existing works still fail to render shapes with flexible head poses and natural facial details (e.g., wrinkles). This limitation is mainly due to two aspects: 1) Collecting training set with detailed 3D facial shapes is highly expensive. This scarcity of detailed shape annotations hinders the training of models with expressive facial animation. 2) Compared to mouth movement, the head pose is much less correlated to speech content. Consequently, concurrent modeling of both mouth movement and head pose yields the lack of facial movement controllability. To address these challenges, we introduce VividTalker, a new framework designed to facilitate speech-driven 3D facial animation characterized by flexible head pose and natural facial details. Specifically, we explicitly disentangle facial animation into head pose and mouth movement and encode them separately into discrete latent spaces. Then, these attributes are generated through an autoregressive process leveraging a window-based Transformer architecture. To augment the richness of 3D facial animation, we construct a new 3D dataset with detailed shapes and learn to synthesize facial details in line with speech content. Extensive quantitative and qualitative experiments demonstrate that VividTalker outperforms state-of-the-art methods, resulting in vivid and realistic speech-driven 3D facial animation

Redox Regulation of Mitochondrial Fission Protein Drp1 by Protein Disulfide Isomerase Limits Endothelial Senescence.

Mitochondrial dynamics are tightly controlled by fusion and fission, and their dysregulation and excess reactive oxygen species (ROS) contribute to endothelial cell (EC) dysfunction. How redox signals regulate coupling between mitochondrial dynamics and endothelial (dys)function remains unknown. Here, we identify protein disulfide isomerase A1 (PDIA1) as a thiol reductase for the mitochondrial fission protein Drp1. A biotin-labeled Cys-OH trapping probe and rescue experiments reveal that PDIA1 depletion in ECs induces sulfenylation of Drp1 at Cys644, promoting mitochondrial fragmentation and ROS elevation without inducing ER stress, which drives EC senescence. Mechanistically, PDIA1 associates with Drp1 to reduce its redox status and activity. Defective wound healing and angiogenesis in diabetic or PDIA1+/- mice are restored by EC-targeted PDIA1 or the Cys oxidation-defective mutant Drp1. Thus, this study uncovers a molecular link between PDIA1 and Drp1 oxidoreduction, which maintains normal mitochondrial dynamics and limits endothelial senescence with potential translational implications for vascular diseases associated with diabetes or aging.This research was supported by NIH R01HL135584 (to M.U.-F.), NIH R21HL112293 (to M.U.-F.), NIH R01HL133613 (to T.F. and M.U.-F.), NIH R01HL116976 (to T.F. and M.U.-F.), NIH R01HL070187 (to T.F.), NIH R01HL112626 (to J.K.), Department of Veterans Affairs Merit Review Grant 2I01BX001232 (to T.F.), AHA 16GRNT31390032 (to M.U.-F.), AHA 15SDG25700406 (to S.V.), AHA 16POST27790038 (to A.D.), and NIH T32HL07829 (to R.C.). We thank Mr. Kyle Taylor at Keyence Corporation for assisting with taking images using the Keyence microscope; Dr. John O’Bryan at UIC for assisting with the BiFC assays; Dr. Leslie Poole at Wake Forest University for providing DCP-Bio1, as well as Dr. Jody Martin and the Center for Cardiovascular Research-supported Vector Core Facility at UIC for amplifying adenoviruses.S

Endothelin-1 (ET-1) promotes a proinflammatory microglia phenotype in diabetic conditions

Diabetes increases the risk and severity of cognitive impairment, especially after ischemic stroke. It is also known that the activation of the endothelin (ET) system is associated with cognitive impairment and microglia around the periinfarct area produce ET-1. However, little is known about the effect of ET-1 on microglial polarization, especially under diabetic conditions. We hypothesized that (i) ET-1 activates microglia to the proinflammatory M-1-like phenotype and (ii) hypoxia/ lipopolysaccharide (LPS) activates the microglial ET system and promotes microglial activation towards the M-1 phenotype in diabetic conditions. Microglial cells (C8B4) cultured under normal-glucose (25 mmol/L) conditions and diabetes-mimicking high-glucose (50 mmol/L) conditions for 48 h were stimulated with ET-1, cobalt chloride (200 μmol/L), or LPS (100 ng/mL) for 24 h. PPET-1, ET receptor subtypes, and M1/M2 marker gene mRNA expression were measured by RT-PCR. Secreted ET-1 was measured by ELISA. A high dose of ET-1 (1 μmol/L) increases the mRNA levels of ET receptors and activates the microglia towards the M1 phenotype. Hypoxia or LPS activates the ET system in microglial cells and shifts the microglia towards the M1 phenotype in diabetic conditions. These in vitro observations warrant further investigation into the role of ET-1-mediated activation of proinflammatory microglia in post-stroke cognitive impairment in diabetes.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Altered peripheral taste function in a mouse model of inflammatory bowel disease

Abstract Increased sugar intake and taste dysfunction have been reported in patients with inflammatory bowel disease (IBD), a chronic disorder characterized by diarrhea, pain, weight loss and fatigue. It was previously unknown whether taste function changes in mouse models of IBD. Mice consumed dextran sodium sulfate (DSS) during three 7-day cycles to induce chronic colitis. DSS-treated mice displayed signs of disease, including significant weight loss, diarrhea, loss of colon architecture, and inflammation of the colon. After the last DSS cycle we assessed taste function by recording electrophysiological responses from the chorda tympani (CT) nerve, which transmits activity from lingual taste buds to the brain. DSS treatment significantly reduced neural taste responses to natural and artificial sweeteners. Responses to carbohydrate, salt, sour or bitter tastants were unaffected in mice with colitis, but umami responses were modestly elevated. DSS treatment modulated the expression of receptor subunits that transduce sweet and umami stimuli in oral taste buds as a substrate for functional changes. Dysregulated systemic cytokine responses or dysbiosis that occurs during chronic colitis may be upstream from changes in oral taste buds. We demonstrate for the first time that colitis alters taste input to the brain, which could exacerbate malnutrition in IBD patients

Diabetes-related sex differences in the brain endothelin system following ischemia in vivo and in human brain endothelial cells in vitro

The endothelin (ET) system has been implicated to contribute to the pathophysiology of cognitive impairment and stroke in experimental diabetes. Our goals were to test the hypotheses that (1) circulating and (or) periinfarct ET-1 levels are elevated after stroke in both sexes and this increase is greater in diabetes, (2) ET receptors are differentially regulated in the diabetic brain, (3) brain microvascular endothelial cells (BMVEC) of female and male origin express the ETA receptor subtype, and (4) diabetes- and stroke-mimicking conditions increase ET-1 levels in BMVECs of both sexes. Control and diabetic rats were randomized to sham or stroke surgery. BMVECs of male (hBEC5i) and female (hCMEC/D3) origin, cultured under normal and diabetes-mimicking conditions, were exposed to normoxia or hypoxia. Circulating ET-1 levels were higher in diabetic animals and this was more pronounced in the male cohort. Stroke did not further increase plasma ET-1. Tissue ET-1 levels were increased after stroke only in males, whereas periinfarct ET-1 increased in both control and diabetic females. Male BMVECs secreted more ET-1 than female cells and hypoxia increased ET-1 levels in both cell types. There was sexually dimorphic regulation of ET receptors in both tissue and cell culture samples. There are sex differences in the stroke- and diabetes-mediated changes in the brain ET system at the endothelial and tissue levels.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Effect of Al Substitution on Visible Short-Wave Infrared Reflectance Spectroscopy (VSWIR) of Goethite and Ferrihydrite

Goethite and ferrihydrite are the two major iron hydroxides, essential mineral constituents in the terrestrial surface system. Aluminum (Al) is the most common substituent in iron hydroxides, and it may significantly change the bulk and surficial physicochemical properties of iron hydroxides. Consequently, a practical and convenient approach is needed to efficiently identify the Al substitution degrees of iron hydroxides in natural occurrences. This study presents a comprehensive investigation of the VSWIR characteristics of laboratory-synthesized Al-substituted goethite and ferrihydrite, to establish diagnostic VSWIR parameters for the identification and quantification of Al substitution levels in iron hydroxides. The findings revealed that Al substitution can affect the band positions (P) of goethite and ferrihydrite at ~650 nm, ~900 nm, and ~1400 nm. The relationships between the Al substitution of ferrihydrite and VSWIR parameters can be expressed as P900 = −0.43 × Al(%) + 931 and P1400 = −0.07 × Al(%) + 1428, while that of goethite can be expressed as P650 = 0.42 × Al(%) + 657 and P900 = 2.29 × Al(%) + 936. The peak fitting results showed that the absorption intensity at 480–550 nm linearly decreases with increased Al substitution. The obtained VSWIR spectra of Al-substituted goethite and ferrihydrite provide a critical supplement to the spectral library for (Al) iron hydroxides, and these VSWIR parameters can be utilized for the semi-quantitative determination of Al substitution in natural iron hydroxide

Discovery of Urinary Proteomic Signature for Differential Diagnosis of Acute Appendicitis

Acute appendicitis is one of the most common acute abdomens, but the confident preoperative diagnosis is still a challenge. In order to profile noninvasive urinary biomarkers that could discriminate acute appendicitis from other acute abdomens, we carried out mass spectrometric experiments on urine samples from patients with different acute abdomens and evaluated diagnostic potential of urinary proteins with various machine-learning models. Firstly, outlier protein pools of acute appendicitis and controls were constructed using the discovery dataset (32 acute appendicitis and 41 control acute abdomens) against a reference set of 495 normal urine samples. Ten outlier proteins were then selected by feature selection algorithm and were applied in construction of machine-learning models using naïve Bayes, support vector machine, and random forest algorithms. The models were assessed in the discovery dataset by leave-one-out cross validation and were verified in the validation dataset (16 acute appendicitis and 45 control acute abdomens). Among the three models, random forest model achieved the best performance: the accuracy was 84.9% in the leave-one-out cross validation of discovery dataset and 83.6% (sensitivity: 81.2%, specificity: 84.4%) in the validation dataset. In conclusion, we developed a 10-protein diagnostic panel by the random forest model that was able to distinguish acute appendicitis from confusable acute abdomens with high specificity, which indicated the clinical application potential of noninvasive urinary markers in disease diagnosis