AI Scientific Illustration Gallery

A Transwell image, 6-well plate.

Style: Clean scientific schematic with a white background, minimal text, and flat vector icons arranged horizontally. Left-to-right flow, emphasizing a scientific approach with no legends and concise text. Layout: Two connected panels: Stage 1 (left) transitions to Stage 2 (right). Stage 1: Electro-Assisted Dark Fermentation (DFMEC). A single anaerobic reactor contains an anode and cathode, connected to a power supply illustrating electron flow from anode to cathode. Inputs: Food waste (C-rich), swine manure (N-rich), optimized C/N ratio, and self-buffering. Inside the reactor: Mixed fermentation broth and SCG-derived biochar coated with a redox-active polymer. Short label: "Zoom in showing Redox-engineered SCG–PEDOT biochar." Key functions (icons): Electron shuttling / DIET. Electrode potential control → NADH/NAD⁺ regulation, indicating that a higher ratio enhances H₂ production, while a lower ratio enhances VFA production. Outputs: H₂ gas (bubbles leaving the reactor). Effluent arrow labeled: "VFA-rich (acetate)". Stage 2: Microbial Electrolysis Cell (MEC).

APPROVED Category: Biomedical Translation: Schematic diagram of a two-stage bioprocess for enhanced hydrogen and volatile fatty acid (VFA) production from organic waste. The diagram features a clean, scientific style with a white background, minimal text, and flat vector icons, illustrating a left-to-right flow. Stage 1: Electro-Assisted Dark Fermentation (DFMEC) A single anaerobic reactor containing an anode and cathode connected to a power supply, indicating electron flow from anode to cathode. Inputs include carbon-rich food waste and nitrogen-rich swine manure. The reactor contains a mixed fermentation broth and redox-engineered biochar composed of spent coffee grounds (SCG) coated with a redox-active polymer (PEDOT). A zoomed-in view highlights the redox-engineered SCG–PEDOT biochar. Key functions: * Electron shuttling / Direct Interspecies Electron Transfer (DIET) * Electrode potential control regulating the NADH/NAD+ ratio, where a higher ratio enhances H2 production and a lower ratio enhances VFA production. Outputs: * H2 gas (bubbles leaving the reactor) * Effluent stream labeled "VFA-rich (acetate)" Stage 2: Microbial Electrolysis Cell (MEC) A two-chamber MEC separated by a membrane. The anode chamber contains an acetate-oxidizing biofilm and exoelectrogenic microorganisms.

APPROVED. Clean, professional scientific schematic depicting a two-panel horizontal layout with a white background, flat vector icons, minimal text, and a left-to-right process flow with color-coded stages. The schematic illustrates Stage 1 (left) and Stage 2 (right) connected by an effluent flow arrow. Stage 1 details Electro-Assisted Dark Fermentation (DFMEC) with a single anaerobic fermentation reactor containing an anode and cathode connected by an external power supply. Inputs include food waste (labeled "C-rich") and swine manure (labeled "N-rich"). Inside the reactor, a mixed substrate slurry and SCG-derived biochar coated with redox-active polymer (labeled "Redox-engineered SCG–PEDOT biochar (DIET & EET)") are shown. The anode and cathode are immersed in the fermentation broth and connected to a small power supply. Key innovations highlighted are "Redox-active electron interface" near the biochar and "Electrode potential control" near the electrodes. The metabolic effect is represented iconically.

1. In vitro CC50, IC50, and plaque assays of the HSP90 inhibitor AUY922 demonstrate its antiviral activity against GCRV. 2. Pre-incubation of cells with AUY922 validates its ability to prevent GCRV infection by inhibiting the expression of genes related to cell membrane receptors, inflammation, and apoptosis. 3. Co-incubation of cells with AUY922 validates its anti-GCRV activity by inhibiting the expression of genes related to cell membrane receptors, inflammation, and apoptosis. 4. Post-incubation of cells with AUY922 validates its therapeutic effect against GCRV infection by inhibiting the expression of genes related to cell membrane receptors, inflammation, and apoptosis. 5. Cell-based assays using inflammation and apoptosis agonists confirm that AUY922 exerts its antiviral activity by inhibiting the expression of inflammation- and apoptosis-related genes. 6. Individual-level validation using techniques such as immunofluorescence, RT-PCR, Western blotting, electron microscopy, and immunohistochemistry confirms that AUY922 inhibits the expression of genes related to cell membrane receptors, inflammation, and apoptosis, thereby exerting its anti-GCRV activity.

I am creating a schematic diagram for a research paper. It depicts FeCu-SAC (Single-Atom Catalyst) as a treatment for acute gouty arthritis. Its functions include clearing uric acid, anti-inflammation, anti-oxidation, and pain relief. It also reduces the levels of inflammatory factors, polarizing macrophages towards the M2 phenotype.

Create an English illustration for the Editorial paper "Phage Therapy in China: Arming the One Health Approach." Depict the role of bacteriophages in human health (nebulized inhalation therapy in a hospital), environmental health (hospital ward environment spray), animal health (drinking water treatment in a duck farm), and plant health (spray in a citrus orchard).

APPROVED The figure should consist of four panels (A–D) arranged sequentially: A: EPO receptor in complex with EPO. B: Insulin receptor in complex with insulin. C: Insulin receptor in complex with IR‑TM peptides. D: Growth hormone receptor in complex with GH. Arrows should indicate ligand/peptide binding and subsequent receptor dimerization/activation. A bottom strip should depict "JAK2: Inactive" versus "JAK2: Active" (or equivalent wording). The overall message is that the IR‑TM peptide activates the IR in a manner analogous to JAK2.

We hypothesize that infiltrating sensory nerves in cervical cancer promote tumor EMT by releasing SP, which binds to the TACR1 receptor on tumor cells and phosphorylates Src protein kinase. Simultaneously, this process reduces CCL7 secretion while promoting IL-33 secretion, establishing an immunosuppressive tumor microenvironment, leading to insensitivity to neoadjuvant chemotherapy combined with immunotherapy.

Figure 2: Key Clinical Evidence in CKRT Dosing and Outcomes Overall Layout: Total dimensions: 850 × 500 px Panel A: x=30, y=55, width 320, height 190 (Dose-Mortality) ⚠️ Revised to binary comparison Panel B: x=365, y=55, width 220, height 190 (Downtime) ⚠️ Revised Panel C: x=600, y=55, width 220, height 190 (NUF rate bar chart) Panel D: x=30, y=270, width 440, height 95 (KDIGO dose scale) Panel E: x=485, y=270, width 335, height 95 (RCA vs. Heparin) Panel A: Dose-Mortality ⚠️ Revised to Binary Forest Plot Important: The Okamoto 2024 study only performed a binary comparison and does not have HR data for multiple dose groups. Design: Forest plot style binary comparison Reference Lines: - HR=1 vertical dashed line: x=200, from y=85 to y=180 - HR scale axis: x=100→300, scale 0.5, 1.0, 1.5, 2.0, 2.5 Above-median group (≥13.2 mL/kg/h): - Label: '≥13.2 mL/kg/h (Above median)', y=115-127 - Data point: Center (200, 120), fill #27ae60 - Annotation: 'Reference' Below-median group (<13.2 mL/kg/h): - Label: '<13.2 mL/kg/h (Below median)', y=155-167 - Error line: HR 1.73 (95% CI 1.19-2.51) - Calculation: With x=200 as HR=1, every 0.5 HR = 50px - HR 1.19 → x=219 - HR 1.73 → x=273 (center position) - HR 2.51 → x=351 (truncated display to x=300) - Horizontal line: x=219 → x=300, color #c0392b 2px - Data point: Center (273, 160), radius 6, fill #c0392b - Annotation: 'HR 1.73 (1.19-2.51)' Key Findings Box: - Location: x=50, y

Please generate a schematic diagram illustrating the mechanism for a biomedical master's thesis, with a professional, concise, and logically clear style. Adopt a left-to-right or center-out layout, distinguishing between "diabetic injury" and "therapeutic intervention" sections. Suggested visual elements and layout: Left side (Injury side): Background labeled "HG", with a dark tone (e.g., light gray). Draw a simplified diagram of a vascular endothelial cell. Above or inside the cell, use "↓" symbols and dashed arrows to indicate two inhibited pathways: Pathway 1 (Top): Labeled "Hippo pathway inhibition", key molecular changes: P-YAP ↓ → YAP nuclear translocation ↑ → leading to "Inflammatory response ↑" (represented by an explosion icon, labeled IL-1β, IL-6, TNF-α ↑). Pathway 2 (Bottom): Labeled "Wnt/β-catenin pathway inhibition", key molecular changes: β-catenin ↓ → CyclinD1 ↓. Below the cell, use downward arrows and crosses to indicate cellular functional consequences: Cell proliferation ↓, Cell migration ↓, VEGF/PCNA ↓. Center (Intervention and turning point): Place a prominent bottle or container icon in the center, labeled "MWE-A", and use a thick green solid arrow pointing to the cell on the right to indicate therapeutic intervention. Right side (Therapeutic recovery side): Background labeled "MWE-A treatment", with a bright tone (e.g., light blue or green). Draw a simplified diagram of a healthy, active endothelial cell. Inside the cell, use "↑" symbols and solid arrows to indicate two activated pathways: Pathway 1 (Top): Labeled "Hippo pathway activation", key molecular changes: P-YAP ↑ → YAP nuclear translocation ↓ → leading to "Inflammatory response ↓" (inflammation icon reduced or disappeared). Pathway 2 (Bottom): Labeled "Wnt/β-catenin pathway activation", key molecular changes: β-catenin ↑ → CyclinD1 ↑. Below the cell, use upward arrows to indicate functional improvement: Cell proliferation ↑, Cell migration ↑, VEGF/PCNA ↑. On the right side of the cell, draw a simplified diagram of the skin wound healing process: A wound that is closing. Draw newly formed capillaries inside the wound (labeled CD31↑). Use icons to represent increased collagen fibers and epithelial layer coverage. Style requirements: Flat or minimalist line style, professional color scheme (e.g., use blue/green to represent activation/benefit, red/gray to represent inhibition/injury). All molecule names, pathway names, arrows, and change trends (↑↓) must be clearly distinguishable. Ensure that causal arrows point clearly, and the overall layout is well-spaced.

Scene Description: Please generate a mechanistic diagram for a biomedical master's thesis, with a professional, concise, and logically clear style. Adopt a left-to-right or center-out layout, distinguishing between "Diabetic Injury" and "Therapeutic Intervention" sections. Visual Elements and Layout Suggestions: Left Side (Injury Side): Background labeled "High Glucose (HG) Microenvironment," with a dark tone (e.g., light gray). Draw a simplified diagram of a vascular endothelial cell. Above or inside the cell, use "↓" symbols and dashed arrows to indicate two inhibited pathways: Pathway 1 (Top): Label "Hippo Pathway Inhibition," key molecular changes: P-YAP ↓ → YAP nuclear translocation ↑ → leading to "Inflammatory Response ↑" (represented by an explosion icon, labeled IL-1β, IL-6, TNF-α ↑). Pathway 2 (Bottom): Label "Wnt/β-catenin Pathway Inhibition," key molecular changes: β-catenin ↓ → CyclinD1 ↓. Below the cell, use downward arrows and crosses to indicate cellular functional consequences: Cell proliferation ↓, Cell migration ↓, VEGF/PCNA ↓. Center (Intervention and Turning Point): Place a prominent bottle or container icon in the center, labeled "Lucilia sericata Larval Extract MWE-A," and use a thick green solid arrow pointing to the cell on the right, indicating therapeutic intervention. Right Side (Therapeutic Recovery Side): Background labeled "MWE-A Treatment," with a bright tone (e.g., light blue or green). Draw a simplified diagram of a healthy, active endothelial cell. Inside the cell, use "↑" symbols and solid arrows to indicate two activated pathways: Pathway 1 (Top): Label "Hippo Pathway Activation," key molecular changes: P-YAP ↑ → YAP nuclear translocation ↓ → leading to "Inflammatory Response ↓" (inflammation icon reduced or disappeared). Pathway 2 (Bottom): Label "Wnt/β-catenin Pathway Activation," key molecular changes: β-catenin ↑ → CyclinD1 ↑. Below the cell, use upward arrows to indicate functional improvements: Cell proliferation ↑, Cell migration ↑, VEGF/PCNA ↑. On the right side of the cell, draw a simplified diagram of the skin wound healing process: A wound that is closing. Draw newly formed capillaries inside the wound (labeled CD31↑). Use icons to represent increased collagen fiber and epithelial layer coverage. Bottom Summary Box: At the bottom of the diagram, use boxed text to summarize the core conclusion: "MWE-A improves endothelial function and accelerates diabetic wound healing by synergistically activating the Hippo pathway (increasing P-YAP) to inhibit inflammation and activating the Wnt/β-catenin pathway (stabilizing β-catenin) to promote proliferation." Style Requirements: Flat or minimalist line style, professional color scheme (e.g., use blue/green to represent activation/benefit, red/gray to represent inhibition/damage). All molecule names, pathway names, arrows

Left: Pipeline 1 (Blue, Near-Term) Cell Therapy Gene Editing CAR-T / NK / TCR-T Multi-gene synchronous editing Near-term realization 👉 Icon: Cell / Lightning Middle: Pipeline 2 (Green, Mid-Term) Hereditary Disease HSC Gene Correction Thalassemia Hemophilia Pipeline-type value 👉 Icon: DNA Repair Right: Pipeline 3 (Purple, Long-Term) iPSC Disease Model & Regenerative Medicine Disease Modeling Drug Screening Regenerative Medicine Long-term valuation ceiling 👉 Icon: Stem Cell / Infinity Symbol Bottom line (must be added): Same underlying platform, multiple market entry points Risk diversification, value superposition

Generate a plasmid DNA backbone comparison diagram. On the left, depict a traditional plasmid backbone as a circular structure, labeled 3000-5000 bp, featuring an antibiotic resistance gene (highlighted in red), an oriC replication origin, and a promoter region, with a gray-orange gradient fill. On the right, illustrate a MiniPlasmid-Pro-1 ultra-compact backbone as a circular structure, labeled 600 bp, containing only a RelB small RNA expression unit (in blue), a replication origin, and a promoter, with a blue-green gradient fill. Connect the two backbones with a bold arrow labeled "85-90% size reduction" and "60-75% cost reduction". The background should be pure white, in a molecular biology textbook style, with a flat design, no shadows, and vector graphic quality.

Protective Role of Atriplex halimus Against Mercury Chloride–Induced Oxidative and Hepatorenal Toxicity in Wistar Rats Abstract Background: Mercury is a highly toxic heavy metal that induces hepatic and renal damage primarily through oxidative stress and tissue bioaccumulation. Medicinal plants may offer protection against mercury-induced toxicity. Objective: This study aimed to characterize the phytochemical composition of Atriplex halimus using GC–MS analysis and to evaluate its protective effects against mercuric chloride (HgCl₂)–induced hepatorenal toxicity in Wistar rats. Methods: The ethanolic extract of A. halimus was analyzed by GC–MS. Forty-two male rats were orally treated for 40 days with HgCl₂ (10 mg/kg/day) with or without A. halimus (400 or 600 mg/kg/day). Mercury accumulation, biochemical markers of liver and kidney function, reduced glutathione (GSH), and histopathological changes were assessed. Results: GC–MS analysis identified linolenic acid (48.05%) and n-hexadecanoic acid as major constituents.

This paper presents a novel 12-transistor transmission gate-based low-power (TGLP12T) SRAM memory cell utilizing carbon nanotube FETs (CNTFETs) for battery-operated implantable medical devices at 32 nm technology. The cell core addresses half-select issues prevalent in conventional SRAM arrays by employing a single-ended read/write architecture, thereby facilitating bit interleaving. The design incorporates stacked NCNTFETs in its pull-down network to enhance write ability and write noise margin, and PCNTFETs in the pull-up path to suppress leakage power. A fully decoupled read path improves the read static noise margin (RSNM), while transmission gate-controlled access transistors and core inverter stacking contribute to reduced dynamic and static power consumption. Comprehensive HSPICE simulations using the Stanford CNTFET model validate the TGLP12T cell's performance.

Provide a comprehensive, research-level overview of the DREB transcription factor signaling pathway in plants. Discuss the functional differences between DREB1/CBF (cold-responsive) and DREB2 (drought and heat-responsive) pathways. Include regulation mechanisms such as post-translational modification, protein stability, transcriptional control, and cross-talk with ABA-dependent stress signaling pathways. Highlight applications of DREB genes in crop stress tolerance.

This review provides a comprehensive, research-level overview of the bZIP transcription factor signaling pathway in plants under salinity stress. It discusses the role of ABA-dependent bZIPs (AREB/ABFs), their regulation by SnRK2 kinases, and the transcriptional control of salt-responsive genes. Furthermore, it includes an analysis of pathway cross-talk with DREB, NAC, MYB, and SOS signaling, post-translational regulation of bZIP proteins, and recent advances in engineering salt-tolerant crops using bZIP genes.