AI Scientific Illustration Gallery

Figure creation: MCF7 cell culture. Seeding followed by treatment with five different cellular stressors: 1. Control, 2. Hypoxia (the flask lid was tightly sealed with parafilm), 3. UV Radiation, 4. Serum Depletion (0.5% FBS), 5. Glucose Starvation (low glucose media), 6. DTT/PFA (2 mM DTT and 25 mM PFA). Cells were cultured inside T25 flasks at 37 °C, 5% CO₂ for 48 hours, reaching 80-90% confluence. UV radiation: cells were subjected to five cycles of UV irradiation (5 minutes) followed by incubation (5 minutes) to stimulate the production of multivesicular bodies. Exosome isolation: Samples were centrifuged at 500 × g for 5 minutes at 4 °C, and the supernatant was removed. The cell pellet was resuspended in 5 mL PBS and centrifuged again at 952 rpm for 5 minutes at 4 °C. The pellet was discarded, and the supernatant was retained. Ultracentrifugation: The clarified supernatant was transferred to ultracentrifuge tubes and spun at 100,000 g for 7 minutes.

Create a figure illustrating the following experimental procedure: MCF7 cells were seeded and then subjected to five different cellular stressors: UV radiation, serum depletion, glucose starvation, DTT/PFA treatment, and hypoxia. This was done to stimulate the production of multivesicular bodies. Exosomes were then isolated via ultracentrifugation, stained with acridine orange, and analyzed via fluorescence microscopy.

Generate an image of clinical peripheral blood in a purple-top tube, with a white background and no specific cells visible in the blood. Also, generate an image of serum in an Eppendorf tube, with a white background.

Please provide a schematic diagram of peripheral blood.

Liver tissue.

You are a world-class visual explanation expert. Please convert this concept into an infographic: [1. Platelets were incubated with acridine yellow (Af) to obtain Af-loaded platelets (Af@Plt), and then incubated with fluorescein diacetate (FDA) to obtain platelets co-loaded with acridine yellow and fluorescein ((Af+Flu)@Plt). 2. (Af+Flu)@Plt were injected into blood vessels and distributed to tumor vessels via blood flow. 3. Under ultrasound stimulation, (Af+Flu)@Plt in tumor vessels were activated and released Af and Flu into the tumor tissue. The released Af and Flu were taken up by tumor cells and tumor-associated macrophages (TAMs). 4. Under ultrasound stimulation, tumor cells and TAMs that had taken up Af and Flu generated a large amount of reactive oxygen species (ROS) inside, resulting in oxidative damage and death, and released Af to surrounding cells. 5. In tumor tissue, low concentrations of Af stimulated M2-type TAMs to exhibit an M1-like anti-tumor phenotype, thereby killing tumor cells. At the same time, Af induced tumor cells to release the 'find me' signal ATP and express the 'eat me' signal CRT on the cell surface, thereby promoting the killing of tumor cells by M1-like phenotype TAMs. In tumor tissue, high concentrations of Af disabled M2-type TAMs, preventing M2-type TAMs from interacting with tumor cells, thereby canceling various pro-tumor functions of M2-type TAMs.]

Generate a high-quality BioRender-style graphical abstract. We need to first deconstruct the key scientific elements of the abstract, transform them into visual language, and then write prompts for AI drawing tools (such as Midjourney, DALL-E 3, Stable Diffusion). ### Part 1: In-depth Abstract Analysis and Visual Decomposition The core logical flow of this paper is as follows: 1. **Background/Input:** * **Object:** Complex Systems, specifically epileptic seizures. * **Features:** High-dimensional data, hidden critical signals. * *Visual elements:* Brain outline, EEG electrode cap, chaotic and dense multi-channel waveform diagram (representing high-dimensional noise data). 2. **Method I - Manifold Learning:** * **Core Technology:** Anisotropic Diffusion Mapping (ADM). * **Purpose:** Construct low-dimensional representations. * *Visual elements:* A funnel-shaped or projection-like graphic that maps the chaotic waveform on the left to a smooth, curved 3D surface (manifold). 3. **Method II - SDE Modeling:** * **Core Technology:** Data-driven stochastic differential equations (SDE), score function, probability density evolution. * *Visual elements:* Arrows or particle flow flowing on the manifold surface, representing the state evolution of the system; or a heat map/cloud moving on the surface. 4. **The Novel Indicator:** * **Theory:** Schrödinger Bridge Theory. * **Indicator Name:** Entropy Production Rate (EP).

Generate a high-resolution schematic diagram for a scientific review article, titled "Clinical Early Warning Network for In Vivo Ion Homeostasis Imbalance." The image should adopt a professional medical visualization style, with a semi-transparent human anatomical outline as the center, clearly presenting the cascade pathway from ion imbalance to organ damage and ultimately to specific clinical emergencies from top to bottom. Surround the top of the image with eight color-coded glowing ion nodes: Na⁺ (dark blue), K⁺ (magenta), Ca²⁺ (orange), Cl⁻ (green), H⁺/pH (purple), HCO₃⁻ (light purple), Mg²⁺ (cyan), and NH₄⁺ (brown). Emit corresponding colored beams from each node, projecting downwards to specific target organs within the human outline (e.g., K⁺ beam focusing on the heart, H⁺/HCO₃⁻ combined beam diffusing throughout the body). The human outline should display major systems such as the brain, heart, lungs, liver, kidneys, and muscles, activated by the ion beams. The beams should turn red at critical imbalance thresholds and extend red arrows pointing to five red warning boxes at the bottom: Malignant Arrhythmia, Acute Brain Injury, Neuromuscular Crisis, Acute Kidney Injury, and Multiple Organ Dysfunction Syndrome (MODS). At the very bottom of the image, arrange six minimalist line-drawn "symptom figures," depicting typical painful postures such as chest pain ECG, headache with head-holding, and hand and foot cramps. The overall composition should highlight the urgency of the "Time Window: Minutes to Hours" and visually convey the core argument that "real-time continuous monitoring of ions as chemical vital signs is key to clinical early warning" through color and flow direction. The style must be rigorous, clear, and academically impactful.

Central Image: Microalgae Cell with Outgoing Arrows to Applications Depict a stylized microalgae cell at the center, representing its foundational role. From the microalgae cell, branch out arrows leading to distinct application areas. One arrow could lead to a depiction of tissue engineering, perhaps showing a regenerating tissue or a scaffold. Another arrow could point to a hydrogel structure, possibly with entrapped cells or drug molecules. Include smaller icons or text along the arrows to represent key benefits like 'Sustainable,' 'Biocompatible,' and 'Bioactive Compounds (Lipids, Proteins, Polysaccharides).' Visual Narrative: From Microalgae to Biomedical Solutions Begin with an image of microalgae in a bioreactor or natural environment, emphasizing their sustainable source. Transition to an illustration of the extraction process, possibly showing key compounds being isolated (e.g., polysaccharides). Next, show these compounds being used to form hydrogels (e.g., alginate interacting).

Network Diagram for Early Warning of Clinical Emergencies Due to Imbalances in Intracellular Ion Homeostasis. Core concept: To reveal how imbalances in seven core ions (Na⁺, K⁺, Ca²⁺, Cl⁻, H⁺/pH, Mg²⁺, NH₄⁺) can trigger multi-system chain reactions, ultimately manifesting as specific clinical emergencies. I. Five-Layer Vertical Structure Top Layer - Ion Projection Source: Seven color-coded source points surrounding the human body, representing seven ions, emitting colored translucent beams. Middle Layer - Human System Outline: A neutral gray human anatomical diagram, receiving all ion beams as an "interaction battlefield." Lower Layer - Comprehensive Emergency Area: Five red warning boxes listing ultimate critical conditions such as malignant arrhythmias, acute brain injury, neuromuscular crisis, acute kidney injury, and multiple organ dysfunction syndrome (MODS). Bottom Layer - Symptom Vignette Column: Six grids, each displaying typical diseases and characteristic painful postures of patients caused by ion imbalances. II. Key Points of the Seven Major Ion Networks Na⁺ (Dark Blue): Osmotic pressure dominance, the beam mainly projects to the brain (cerebral edema/atrophy) and the whole body. K⁺ (Magenta): Cardiac electrophysiological activity arbiter, the beam connects the heart (arrhythmia) and muscles (weakness/paralysis). Ca²⁺ (Orange): Muscle contraction switch, the beam connects neuromuscular (spasm/weakness), heart (QT changes), and kidney (stones). H⁺/pH (Purple): Enzyme activity lifeline, radial beams connect all organs, leading to widespread dysfunction. Cl⁻ (Green): Low-key coordinator, the beam emphasizes its association with Na⁺ (electrical neutrality) and pH (acid-base balance). Mg²⁺ (Cyan): Ion channel gatekeeper, the beam connects the heart (torsades de pointes) and neuromuscular system, and regulates K⁺ and Ca²⁺ with dashed lines, with a warning note: "Refractory imbalance? Check blood magnesium first!" NH₄⁺ (Brown): Liver-kidney-brain axis toxin, the beam originates from the liver, passes through the kidney, and the core path directly penetrates the blood-brain barrier towards the brain (hepatic encephalopathy). III. Bottom Symptom Vignette Column (Key Clinical Anchors) Presenting typical painful postures with minimalist stick figures, intuitively connecting mechanisms with bedside manifestations: Hyperkalemia: Supine stick figure, ECG showing cardiac arrest → "Premonition of cardiac arrest." Hyponatremic Cerebral Edema: Stick figure holding head with both hands, expressing pain → "Explosive headache." Hypocalcemic Tetany: Stick figure with forearm in "obstetrician's hand" position → "Carpal spasm." Metabolic Acidosis: Forward-leaning sitting posture, deep and rapid breathing → "Kussmaul breathing, fatigue." Arrhythmia/Heart Failure: Stick figure clutching chest and curling up, expressing extreme pain → "Palpitations, chest pain." Kidney Failure/Stones: Bending over and clutching waist, expressing pain → "Waist pain, anuria." IV. Global Warning and Value Top Warning: "Seven Signs of Chemical Life: Any imbalance can trigger a systemic domino effect. Time window: Minutes to hours." This diagram achieves a complete narrative loop from ion mechanisms to organ interactions and then to specific symptoms.

1. Overall Layout: A centered circular closed loop, equally divided into four quadrants. Four segments are equidistantly distributed clockwise on the ring, connected by light blue arrows, forming a complete cycle. 2. Four Core Segments (clockwise): First Segment (12 o'clock position): Agricultural Waste Input Icon: A simple corn cob outline icon. Label: "Agricultural Waste" (e.g., corn cobs). Visual: The icon is filled with light green, symbolizing nature and raw materials. Second Segment (3 o'clock position): Biomanufacturing Core Icon: A combination icon of a flask and a double helix DNA, representing synthetic biology fermentation. Label: "L-Lactic Acid Production." Visual: The icon is filled with blue, symbolizing technology and manufacturing. Third Segment (6 o'clock position): Material Synthesis Icon: A polymer chain structure icon composed of "PLA" letters. Label: "PLA Synthesis." Visual: The icon is filled with dark blue, symbolizing materials and polymerization. Fourth Segment (9 o'clock position): End Products Icon: An outline icon of a degradable lunch box or shopping bag. Label: "Green End Products." Visual: The icon is filled with green, symbolizing environmental protection and finished products. 3. Connections and Dynamics: Each segment is connected by simple curved arrows, with the arrow color being light blue, indicating the direction of material and value flow. In the center of the ring, a circular arrow icon or the words "Green Material Ecology" can be added to highlight the theme. 4. Style and Color Scheme: Background: Pure white. Lines: All graphics use thin solid line borders, without shadows, maintaining a flat design. Color Scheme: Green (#4CAF50): Represents agriculture and environmental protection. Blue (#2196F3): Represents technology and manufacturing. Light Blue (#87CEEB): Used for connecting arrows. Font: Use a sans-serif font (such as Microsoft YaHei, Arial), with small and clear label text.

I want to create a simplified flowchart outlining the following steps: single-cell sequencing of corneal repair in rodents and non-human primates; cross-species analysis of cell type homology; and identification of differentially expressed genes in the early stages of the repair process.

FGF1 knockout mice exhibit impaired cognitive function. (1) Spontaneous alternation rate and total arm entries in the Y-maze test were significantly decreased in FGF1-/- mice. In the passive avoidance test, the time spent in the dark chamber on the second day was significantly reduced in FGF1-/- mice. The novel object recognition test indicated impaired short-term memory in FGF1-/- mice. Behavioral experiments demonstrated a decline in cognitive abilities in FGF1-/- mice compared to the wild-type group. (2) Transcriptomic analysis of the hippocampus revealed that FGF1 knockout leads to complex disorders in the nervous system, immune system, and lipid metabolism. (3) Lipidomic analysis of the hippocampus suggested lipid remodeling after FGF1 knockout, and related network analysis indicated that ceramide Cer(d18:1/22:0) plays a central role in related glycolipid metabolic pathways. (4) FGF1-/- mice showed activation of brain inflammatory responses, activation of the NF-κB/NLRP3 neuroinflammatory pathway, increased expression of brain inflammatory factors (IL-1β, TNF-α, IL-6), and impaired antioxidant stress function. Simultaneously, the blood-brain barrier was damaged, and peripheral immune cells invaded the central nervous system. (5) Neuronal expression was decreased and neuronal synaptic function was impaired in FGF1-/- mice. (6) Myelin regeneration function was impaired in FGF1-/- mice.

Schematic Title: Schematic Diagram of Microneedle Patch Preparation Process Overall Style and Layout: Style: Simple, modern, with technological line illustrations or flat vector graphics. Use a refreshing color scheme, mainly blue, gray, and white, with key parts highlighted in orange or green. Layout: A horizontal flowchart from left to right, including 4 core steps. Each step is clearly marked with a numbered module (Step 1-4). Detailed Description of Steps: Step 1: Mold Casting Scene: On the left is a transparent/translucent polymer microneedle mold (such as a PDMS mold), with a regularly arranged array of inverted pyramid or conical pits visible on its surface. Action: A pipette or dropper is dropping a drop of viscous, translucent mixed solution onto the surface of the mold. The solution can be symbolically dotted with tiny nanoparticles (NPs) to represent DNase-PDA@C-176 NPs. Label: Label the solution as "HA and DNase-PDA@C-176 NPs mixed solution". Label the mold as "Microneedle Mold". Step 2: Vacuum Filling Scene: The mold is placed in a transparent vacuum chamber. State: The solution on the surface of the mold has spread and covered the entire mold area. A vacuum pump icon (or a simple downward arrow indicating air extraction) is connected above the vacuum chamber. Key Visual: In the pits of the mold, use an enlarged partial cross-sectional view to show that the solution is being drawn down under the action of vacuum negative pressure, completely filling every tiny corner of the pit and expelling all air bubbles. A few small upward air bubble arrows can be used to indicate the dynamic process of exhaust. Label: "Vacuum Filling" or "Vacuum Degassing". Step 3: Drying and Curing Scene: The mold is transferred to a dry environment, such as being placed under a gentle warm air flow (indicated by curved arrows) or placed in a "drying oven" icon. State: The moisture in the solution in the mold evaporates, the volume shrinks, and finally solid needles are formed in the mold pits. A partial cross-sectional view can be used again to compare: from pits filled with liquid to solid needles. Label: "Drying/Curing". Step 4: Demolding and Finished Product Action: A hand or a robotic arm is carefully peeling/removing a formed microneedle patch substrate (a transparent polymer backing) from below. Finished Product Display: The peeled patch is displayed completely. Hundreds of tiny conical needle tips stand neatly on the patch substrate, forming a perfect array. Multi-angle Display (Optional): Main View: Complete patch. Side View/Magnified View: Shows the sharp needle tip and complete shape of a single microneedle, with dimensions labeled as "Height: 1000 μm, Base Width: 600 μm". Top View (Illustration): Shows the regular arrangement of microneedles, such as a "10x10 array" or similar. Final Label: Label the finished product as "DNase-PDA"

A pipette with a tip attached.

Six jars of water kefir, two units of honey, two units of molasses, and two units of brown sugar were prepared and covered with cheesecloth.

Methods: Adult male Wistar rats were subjected to diffuse severe traumatic brain injury (TBI) using the Marmarou weight-drop model under anesthesia. Thirty minutes post-injury, pinocembrin (Pino) was administered intraperitoneally at doses of 25, 50, and 100 mg/kg. Neurological function was assessed using the Veterinary Coma Scale, beam walk, and beam balance tests at baseline, immediately after recovery from anesthesia, and at 24, 48, and 72 hours post-trauma. Cerebrospinal fluid (CSF) samples were collected for ELISA analysis of matrix metalloproteinase-9 (MMP-9), and brain tissues were fixed in 10% formalin for histological evaluation using hematoxylin and eosin staining. Results: Severe TBI induced significant neurological deficits, increased cerebral edema, disruption of blood-brain barrier (BBB) integrity, and impaired balance and motor performance. Treatment with pinocembrin at 25 and 50 mg/kg significantly attenuated these pathological changes compared with controls (p < 0.001). These doses also reduced cerebrospinal fluid MMP-9 levels, which were markedly elevated following TBI.

Subject: Experiment Flowchart of Bacterial Activation and Phage Treatment of Biofilm Formation Style: Concise, scientific experimental flowchart, black lines on a white background, clear icons Requirements: Use clear arrows to connect each step. All key nouns must be represented by icons/pictures, and ensure the icons are easy to understand. The process layout is from left to right and from top to bottom, with clear logic. Steps and Icon List: Start [Icon: Stock tube] (containing target bacteria) Use [Icon: Inoculation loop] to pick up bacterial solution from [Icon: Stock tube]. Perform [Icon: Streak plating] on [Icon: 90mm petri dish] (containing solid medium) to activate bacteria. Incubate in an incubator until [Icon: Single colony] grows. Use [Icon: Inoculation loop] to pick a [Icon: Single colony]. Inoculate the picked colony into [Icon: Erlenmeyer flask] containing [Icon: 2216E liquid medium] and shake culture. Measure periodically until [Icon: Spectrophotometer] shows the bacterial solution [Icon: OD600=0.1]. Branch point: Dispense the bacterial solution into two new, sterile [Icon: Erlenmeyer flasks]. Control group: Keep one [Icon: Erlenmeyer flask] as is. Experimental group: Add [Icon: Bacteriophage] to the other [Icon: Erlenmeyer flask]. Use [Icon: Pipette] to transfer the liquid from the two Erlenmeyer flasks to the wells of 4 [Icon: 24-well plates] respectively (the liquid from each Erlenmeyer flask corresponds to 2 well plates). Parallel processing: Place these 4 [Icon: 24-well plates] in [Icon: Different environments] (e.g., different temperatures or shakers) and incubate for [Icon: 24 hours]. After incubation, remove all well plates. Collect the [Icon: Biofilm] formed in each well plate. Place the collected [Icon: Biofilm] samples in [Icon: 1.5ml centrifuge tube]. End (for subsequent analysis). Layout: Please ensure that steps 1-7 are arranged vertically, and after step 8 (dispensing), the control group and the experimental group expand downwards in parallel, and steps 9-13 converge again.

APPROVED This is the abstract of my project proposal. Please generate a scheme for it. Abstract: Asymmetric segregation of protein damage and "aged proteins" during cell division is considered a key mechanism in the initiation of aging and cellular rejuvenation. However, existing studies mainly rely on observing a few fluorescently labeled molecules, lacking the ability to globally analyze at the molecular level and making it difficult to distinguish between new, old, and damaged proteins. To address these issues, this project proposes to use human cells as a model, combining live-cell fluorescence imaging, metabolic isotope labeling, and single-cell proteomics to systematically study the differential segregation patterns of protein abundance, new/old ratios, and damaged components between sister daughter cells during cell division. By constructing a SNAP-Omp25 mitochondrial temporal labeling system, we aim to capture asymmetric segregation events and perform Astral DIA single-cell proteomic analysis on strictly paired sister daughter cells to obtain high-resolution molecular readouts. Furthermore, we will introduce machine learning methods to extract stable asymmetrically segregated proteins and functional modules, and verify their regulatory roles through genetic and pharmacological interventions. This study will elucidate the molecular mechanisms of protein homeostasis resetting and damage isolation in human cells, laying the foundation for understanding aging mechanisms and intervention strategies for related diseases.

Title: Surface Chemistry Orchestrates the Immunological Identities of Nanoplastics via Protein Corona Formation Scientific Question: How do the surface functional groups of nanoplastics (PS) exposed via the bloodstream specifically encode the protein corona formed in serum? How does this differentiated protein corona, generated by surface chemistry, determine the immun recognition patterns, cellular responses, and ultimate toxic effects of nanoparticles in mice? Methods: First, 200 nm polystyrene nanoparticles with carboxyl (PS-COOH), amino (PS-NH2), and unmodified (PS) surface modifications were selected and characterized. They were then incubated with mouse serum in vitro, and proteomic analysis was performed using liquid chromatography-tandem mass spectrometry to identify the differential expression of proteins in the three protein coronas. This comparison clarified the specific regulatory effects of surface functional groups on protein corona composition. Subsequently, a blood exposure model (tail vein injection) was established, and transcriptome sequencing was performed on mouse peripheral blood cells at the single-cell level. Differential expression gene analysis and KEGG pathway enrichment analysis were conducted on the sequencing data for each cell subpopulation to systematically map the immune cell-specific transcription profiles induced by nanoplastics with different protein coronas. Finally, using mouse macrophages as an in vitro model, bare particle groups and pre-coated protein corona particle groups were established. Cell viability was assessed using the CCK-8 method, cellular uptake efficiency was quantified by flow cytometry, and inflammatory cytokine levels were measured by ELISA. Spearman correlation analysis was performed to integrate protein corona composition data with cellular function data, establishing a quantitative relationship between key protein adsorption and biological effects, with the aim of revealing the complex interaction mechanisms between surface functional groups, protein adsorption, and immune responses. Conclusions: The study demonstrates that surface charge is a crucial factor in regulating protein corona composition. Carboxylation leads to the specific enrichment of complement and coagulation proteins, while amination primarily adsorbs apolipoproteins and albumin. This specific adsorption is not random but is driven by molecular properties such as surface potential and protein isoelectric point, achieving a precise conversion of surface chemical information into biological molecular identity. PS-COOH with a complement protein corona is efficiently recognized and endocytosed by macrophages through complement receptors and other pathways, specifically activating the NF-κB signaling axis and driving classical inflammatory pathways such as TNF and IL-17, triggering a strong immune response. In contrast, PS-NH2 with an apolipoprotein corona mimics endogenous lipoprotein particles, reducing rapid clearance by the endothelial phagocytic system, prolonging blood half-life, and primarily inducing upregulation of mitochondrial respiratory chain genes and disruption of oxidative phosphorylation pathways.

Deep Proteomics-Discovered Molecular Identities Reveal Biological Functions of Nanoparticle Protein Corona Key Scientific Questions: 1. Missing Causal Mechanisms: How do the key physicochemical properties of nanoparticles (surface charge, PEGylation, morphology, material) systematically and causally determine their protein corona composition, and in turn, regulate biological fates such as cellular uptake and immune recognition? 2. Data Resource Bottleneck: How can we overcome the fragmentation and low quality of existing public proteomics data to establish a high-quality, standardized nanobio interaction database that can support reliable mechanism discovery and model prediction? Research Methods: This study employs an integrated "data mining-guided experimental construction" strategy. First, a literature-mined nanoparticle protein corona database (LM-NPC-DB) was constructed through text mining and literature data integration, systematically evaluating the field's research paradigm and data quality defects. Based on this analysis, a standardized nanoparticle library covering 42 different materials, charges, PEGylation states, and morphologies was rationally designed and synthesized. Subsequently, a high-quality in-house nanoparticle protein corona database (IH-NPC-DB) was constructed by strictly following uniform standard operating procedures. This database, with its high reproducibility, high protein coverage, and minimized missing values, serves as the core data foundation for this study. On this basis, combined with bioinformatics analysis (differential protein analysis, pathway enrichment, network analysis), machine learning models (predicting morphology-specific adsorption), and functional cell experiments (such as using gene knockout cell models to verify specific uptake pathways), the quantitative relationship between nanoparticle properties, protein corona composition, and biological effects was systematically decoded. Conclusions: This study is expected to establish and validate a clear causal framework of "nanoparticle properties → protein corona composition → biological fate." Specific conclusions include: 1. Surface charge guides protein adsorption through electrostatic-hydrophobic synergistic effects. Negatively charged particles enrich adhesion proteins and mediate efficient cell uptake via Itgav, while positively charged particles preferentially bind to apolipoproteins. 2. PEGylation actively reduces the adsorption of immune-related proteins such as complement/coagulation factors, reconstructing the protein corona to achieve "immune stealth" and effectively inhibit macrophage inflammatory responses. 3. Particle morphology shapes a unique protein adsorption fingerprint. Spherical particles enrich adhesion-related proteins, while rod-shaped particles exhibit high immunogenic potential, both achieved through different physical interactions and interfacial geometric effects. 4. Different materials exhibit complementary protein adsorption profiles, which can be used as "molecular amplifiers" to specifically enrich low-abundance disease biomarkers, providing a theoretical basis for constructing multi-material combined liquid biopsy panels. Ultimately, this study not only provides a standardized database (IH-NPC-DB) that surpasses the quality of existing public data, but also enables rational...

"Rich and mellow" is a core term used to describe the taste of high-quality green tea. "Richness" mainly refers to the intensity and thickness of the tea soup, which is a direct reflection of the high content of water extract, rich in tea polyphenols, caffeine and other substances that provide a strong sensory impact. "Mellow" emphasizes the mellowness and coordination of the tea soup, referring to the moderate bitterness and astringency, balanced with freshness and sweetness, resulting in a comfortable aftertaste in the mouth after swallowing, rather than a stimulating astringent sensation. It is not limited to a single taste dimension, but is the product of the synergistic effect of multi-sensory signals such as taste, smell and oral tactile sensation, and its perceived physiological basis covers a multi-dimensional complex mechanism. First, from the perspective of taste, the formation of a rich and mellow taste is closely related to basic tastes such as sweetness and umami, and sweetness is the cornerstone of its core taste experience. For example, during the long-term withering process of white tea, the content of soluble sugar inside the tea leaves accumulates significantly, and the sweetness increases, and the mellow and smooth taste also follows, which together creates its unique rich and mellow flavor [4]; sweetness perception is mediated by the T1R2/T1R3 heterodimeric receptor, which makes the brain feel pleasant about the stimulation of sweetness, which further enhances the overall perception of the rich and mellow taste. In addition, there is a two-way interaction between sweetness and salty, sour, bitter, umami and other tastes, such as adding sugar and milk to coffee to adjust the tribological properties of the system, weakening the bitterness while enhancing the sweetness and mellowness, which confirms the regulatory effect of taste interaction on the rich and mellow flavor. Second, the sense of smell plays an indispensable synergistic role in the perception of rich and mellow taste. Volatile compounds in food combine with olfactory receptors through the orthonasal and retronasal olfactory pathways, and the rich aroma signals generated are integrated with taste information in the cerebral cortex to form a complete flavor perception. For example, the sweet floral, warm fruity, or aged woody aromas in tea drinks can complement the taste signals and significantly enhance the overall richness and mellowness [9]; the rich and mellow experience of coffee is also inseparable from complex volatile components, and different roasting degrees create differentiated flavors, such as the chocolate and caramel aromas produced by medium-roasted coffee beans, which not only enrich the flavor level, but also enhance the rich and mellow texture through the synergistic effect of aroma and taste. Third, oral tactile sensation is the key physical basis for the perception of rich and mellow taste, and its core is directly related to the physical properties of food such as texture, viscosity, smoothness and granularity. For example, the rich and mellow taste of dairy products is derived from the synergistic effect of their milky aroma, milk flavor, viscosity and smoothness, in which viscosity and smoothness can directly enhance the oral tactile perception of richness and mellowness. Relevant studies have made it clear that creaminess and smoothness are the core dimensions for evaluating the rich and mellow taste of food, and the difference in their physical properties will directly affect the perception intensity and comfort of the rich and mellow taste. In summary, the perception of rich and mellow taste is a complex physiological process of multi-sensory synergistic integration of taste, smell and oral tactile sensation, which relies on the specific recognition of multiple chemical components by taste receptors, the precise capture of volatile aroma substances by the olfactory system, the intuitive perception of the physical texture of food by oral tactile sensation, and the integration, processing and comprehensive analysis of these multi-source sensory signals by the cerebral cortex.

Illustrate the growth process of a mung bean from seed to the emergence of two true leaves, spanning two months, and culminating in yellowing leaves and the development of a few seed pods.

Lats1-AKO and Lats1^f/f^ mice were fed a high-fat diet for 12 weeks, followed by local injection of AAV-BST2 into subcutaneous adipose tissue. The high-fat diet was continued until week 24. Please draw a schematic diagram of the experimental design.