Coming to a city near you. Stay up to date with the new breeders and unique special events.
26Yesterday
Back to Explore
Science
Dive into scientific discoveries and technological advancements
Created by users on Jellypod • Updated daily
Join us to learn more about the Pittsburgh Reptile Show & Sale the largest monthly reptile expo in Western Pennsylvania
86 days ago
The Honors Element is a podcast created for Penn State Honors General Chemistry students, exploring the fundamental ideas that shape how we understand the chemical world. Each episode connects core concepts to real-life applications while preparing students for upcoming lectures.
131 week ago
Developed by cognitive archaeologist Derek Hodgson, the Neurovisual Resonance Theory proposes that early humans created "art" because certain visual patterns—like symmetry and repetitive marks —resonated with the structure of their brains. In other words, our ancestors weren’t just painting what they saw, they were painting what their brains were wired to respond to. This resonance comes from the way our visual cortex processes information. Over millions of years, humans evolved to detect movement and forms in complex environments. These survival skills shaped the way we see—and ultimately, the way we create.
22 weeks ago
Cells: Cell Definitions Photosynthesis Structure of the leaf: Waxy cuticle: thin, waterproof layer that reduces water loss Upper Epidermis: Transparent protective layer, allows light to pass through Palisade mesophyll: Packed with chloroplasts Spngy Mesophyll: Allows for gas exchange Vascular bundle: Xylem for water, phloem for nutrients Lower epidermis: Where most stomata are found Include word equation (Water + Carbon Dioxide (sunlight)→ Oxygen + Glucose) Include chemical equations (6CO2 + 6H2O → 6O2 + C6H12O6) Organelles: a specialised, membrane-bound structure within a eukaryotic cell that performs a specific function, analogous to an organ in a larger organism Stroma is transparent: lacks chlorophyll, contains nutrients and water How do plants get their reactants? Water: Through osmosis in the root hair cells Carbon dioxide: Through diffusion in the stomata The process of photosynthesis? LDR: Water is broken down into H+ ions, electrons and oxygen gas. Uses light energy to produce NADPH and ATP in the thylakoid membrane LIR: Uses a series of reactions to bind H+ ions to CO2 to produce glucose using the NADPH and ATP from LDR in the stroma Factors that affect the rate? Less water → less H+ ions, less ATP → less glucose Less CO2 → Less glucose Limiting factors → increasing one will increase the rate TO A POINT where one will become limiting Less sunlight → LDP cannot function High Temperature = faster particles, too high = denature enzyme Enzymes? High temperature → Permanent Denature Low temperature → Slows the rate of reaction Denature → No ATP produced → no glucose produced → photosynthesis stops Adaptations? Clear membrane → Allows for better light absorption in chloroplasts Closer to the edge of the cell for better absorption Thylakoid stacks → Increases surface area for absorption Stroma close to grana → close proximity leads to a faster transfer of products Shade leaves thin → to maximise surface area for absorption they have thinner cuticles and also less palisade cells to minimise water loss Respiration Anaerobic (Glucose → Lactic acid + 2 ATP) Cytoplasm Advantages of Anaerobic? Does not require oxygen Faster Disadvantages of Anaerobic? Less ATP produced Produces toxic byproducts Why can only carry out Anaerobic respiration for short periods of time? Because the production of lactic acid build up causes fatigue and Aerobic (Oxygen + Glucose → Water + Carbon dioxide + 36 ATP) Glycolysis is similar to Anaerobic respiration. Krebs cycle: Mitochondrial matrix ETC: Mitochondrial cristae Advantages of Aerobic? Produces 18x more ATP Does NOT produce toxic byproducts Disadvantages of Aerobic? Slower Requires oxygen Mitochondria number? The higher the mitochondria number in the cells = the more energy the cells use Cell Cycle Checkpoints to ensure that the cell is healthy (not cancerous) Ensures that the DNA is safe to replicate Cell grows DNA replication Mitosis/Meiosis How does the cell cycle prevent mutations? The cell cycle has checkpoints that can ensure that the cell is functioning properly. This allows for the process to stop growing the cell, in order to prevent the cell from possibly being cancerous or harmful to the organism. DNA replication BEFORE Mitosis/Meiosis Purpose: “to produce two identical copies of a cell's DNA, ensuring that each new daughter cell receives a complete and accurate set of genetic instructions during cell division” DNA: Wrapped around histones Double helix Stores genetic information Antiparallel strands Deoxyribose (5-carbon sugar) + Phosphate group + nitrogenous base Leading (5’ to 3’) and lagging strands (3’ to 5’) Helicase unzips the DNA strand New nucleotides bind to the exposed strand from 5’ to 3’ DNA Polymerase uses Complementary base pairing (A to T, C to G) Leading and lagging strands Lagging strand in sections called Okasaki fragments Ligase binds the fragments to make a complete strand Semi-conservative replication (one old and one new strand) Name the enzymes? Helicase, DNA polymerase, ligase Mitosis Prophase: Chromosomes condense and become visible Metaphase: Sister chromatids line up at the cell equator Anaphase: The spindle separates the chromosomes Telophase: The cells begin to split as the cytoplasm divides Cytokinesis: 2 complete identical daughter cells are formed Diffusion Passive Simple diffusion Facilitated Diffusion Osmosis → Hypotonic to hypertonic Hypertonic Hypotonic e.g. root hair cells for osmosis, alveoli for gas exchange, ion pumps in neurons. Active Active transport e.g. Ion pump Factors that affect the rate? Surface Area Concentration Temperature Distance of diffusion Why Active transport can bring in more substances? Because the rate of facilitated diffusion gets slower the closer the concentration of the substance inside and outside the cell is (equilibrium), while active transport can continue to go against the concentration gradient because it uses energy. Enzymes Substrate specific Made up of proteins and hydrogen bonds May require co-factors or co-enzymes Co factors = Inorganic molecules (usually metal ions) Co enzymes = organic molecules. Reduce activation energy Catabolic = Break down Anabolic = Build up Induced fit model Rate of enzymes? Enzyme concentration Substrate concentration Temperature Low temperatures → Slow down High temperature → Denature Presence of inhibitors Competitive → Bind directly to the active site Non-competitive → Binds to the outside, changes active site shape pH (un optimal pH can break the hydrogen bonds) Denature = Lose its function Genetic Variation Meiosis Purpose → to produce gametes with half the chromosome number, restoring diploidy at fertilisation. Fertilisation itself also creates variation (random fusion of gametes). Prophase 1: Chromosomes condense and become visible Crossing over - new combination of ALLELES (not genes) Metaphase 1: Homologous chromosomes line up at at cell equator Independent assortment - each gamete only receives one chromosome Anaphase 1: The spindle separates homologous chromosomes Telophase 1: The cells begin to split as the cytoplasm divides Metaphase 2: Chromosomes line up at the equator Anaphase 2: Chromosomes are pulled apart by spindle fibers Segregation Telophase 2: The cells begin to split as the cytoplasm divides Cytokinesis: 4 unique daughter cells are formed Where is variation? Crossing over → increases the chance of recombination, resulting in different phenotypes from the parents Independent assortment → Mixes the mothers' and fathers' genes Segregation → mixes the mothers' and fathers' alleles Fertilisation → combination of 2 unique gametes Genes and alleles Homozygous Dominant, Homozygous Ressesive, Heterozygous Different ways of dominance? Co-dominance - Both alleles FULLY expressed. Ratio: 1:2:1 Incomplete dominance - Blend of both alleles. Ratio: 1:2:1 Complete dominance - Only the dominant allele is expressed. Ratio 3:1 Explain the differences between genotype and phenotype ratios? Because the incomplete/co-dominace results is a blend and splotch expression of the alleles, leading to 3 different phenotypes rather than the 2 possible phenotypes from the 3 genotypes in complete dominance. Linked genes: genes found on the same chromosome Why does independent assortment not affect linked genes? Unless crossing over has occurred, the genes are on the same chromosome and cannot be separated. Why does crossing over not affect non-linked genes? Because the genes are already on each chromosome, they cannot be crossed over. Sex-linked genes: genes only found on X or Y chromosomes (x linked is more common in males) Why is it more common for males to inherit it compared to females? Because males only have 1 X chromosomes, and females have 2, meaning if it is recessive, the female needs to have 2 copies of the allele while the male still only needs one. Multiple alles: When there is more than 2 alleles for a single gene Lethal alleles: Alleles that significantly reduce the lifespan of the organism that posses them. Ratio 2:1 Charts: Pedigree: Looking at a specific family for inheritance Monohybrid inheritance: inheritance of 1 gene (2 alleles) Dihybrid inheritance: inheritance of 2 genes (4 alleles) Effects on Gene pool Allele frequency Fixed alleles: 0% or 100% frequency Founders effects Bottleneck effect Genetic drift Mutations (original and only source of new alleles) Natural selection Population size: Smaller population more susceptible to changes Gene flow How are new alleles introduced and spread in a population? Mutations in the base sequence is the only new source of alleles. Natural selection selects advantageous alleles by those organisms that posses those advantageous alleles living long enough to reproduce, spreading their alleles to their offspring. This increases the allele frequency in the gene pool. Beneficial alleles increase in allele frequencies, harmful alleles decrease in allele frequency Explain Founder's effect, genetic drift, bottleneck effect and natural selection Gene Expression Genetic variation: the naturally occurring differences in alleles (versions of genes) and genetic information within a population or species The process by which the information in a gene is used to synthesise the other product. Transcription Promoter region, coding region, terminator region RNA polymerase matches the nucleotides to the template (anti-sense) strand in the complementary base pairing rule of A-U, C-G. Not the coding (sense) strand. Editing phase Introns (non coding parts of mRNA) are spliced out and the exons (coding parts of mRNA) are joined together Translation When mRNA goes through the ribosome, and the tRNA is able to match the codon on the mRNA to complementary anticodon on the tRNA, until it reaches a stop codon, to ensure the correct amino acid sequence Point mutations: Substitution → No change in reading frame Deletion, Insertion → Big change in reading frame, which can alter the protein, removing its intended function. Same-sense: No new amino acid is formed Mis-sense: A new amino acid is formed Non-sense: No new amino acid is formed Protein structure: Primary: Polypeptide chain, peptide bonds Secondary: Alpha jelix or beta sheets, hydrogen bonds Tertiary: 3D structure, di-sulphide bridges, hydrogen bonds, ionic bonds Quantenary: Combination of tertiary structures Types of proteins Enzymatic, structural, regulatory, transport Metabolic pathways: Enzyme-catalysed reactions where the product of one of the reactions is the reactant of another reaction. When an excess of one product is produced, it can inhibit a previous reaction intentionally to regulate, or unintentionally due to faulty gene. Cycle metabolic pathways always produce the starting reactant as the final product How can 2 parents have a metabolic mutation but offspring does not? As long as the offspring inherits one functioning allele, it is ables to go through the full metabolic pathway. Mutagens: environmental factor that causes a mutation eg carcinogens (cancer causing) Mutations are PERMANENT Epigenetic markers can control the expression of genes (whether they are transcribed or not, based on methyl and acetyl groups). These can be controlled through external or internal factors that do not change the genotype. Cline is a gradual change in the phenotype over an environmental gradient Type of RNA Structure Function Stage mRNA Short, unstable, single-stranded RNA, corresponding to a gene encoded within DNA Serves as intermediary between DNA and protein; used by ribosome to direct synthesis of protein it encodes Both tRNA Short (70-90 nucleotides), stable RNA with extensive intramolecular base pairing; contains an amino acid binding site and an mRNA binding site Carries the correct amino acid to the site of protein synthesis in the ribosome Translation rRNA Longer, stable RNA molecules composing 60% of ribosome’s mass Ensures the proper alignment of mRNA, tRNA, and ribosome during protein synthesis; catalyzes peptide bond formation between amino acids Translation Why is mRNA unstable while the others are stable? mRNA is temporar and easy to degrade (only lived for purpose and cna be controlled to save energy) tRNA and rRNA is structurally protected and reused many times (saves cell energy from remaking them) What are 3 similarities between DNA and RNA? Both are Nucleic Acids - made of nucleotides, sugars, phosphates and bases Both are used in the cell to undergo protein synthesis - DNA for genetic information and RNA for translation of DNA triplets to RNA transfer and translate it into proteins Both use complementary base pairing to create new strands - A-T or A-U and C-G What are 3+ differences between DNA and RNA? DNA cannot leave the nucleus, and RNA can - because DNA needs to be kept safe inside the nucleus DNA uses Thymine and RNA uses Uracil - 2 different bases that bind to Adenine DNA is double-stranded, while RNA is single-stranded DNA uses Deoxyribose and RNA uses Ribose How can mutations in DNA result in faulty metabolic pathway? When a mutation in the DNA occurs, the proteins synthesis of that gene can turn the gene into a protein that forms an enzyme. If there was any mutation that resulted in a different protein forming, the function of the enzyme would not be able to be achieved, therefore, the reactants cannont be converted into the products if there is not correct gene/allele for the enzyme. The product would not be produced. The organism needs atleast one functioning allele to code for the correct enzyme, in order for the enzyme to function. What happens if a premature stop codon is produced? A premature stop codon causes translation to end too early, producing a shortened (truncated) protein. Because it is incomplete, it cannot fold into the correct shape, so it loses its function. This loss of function is significant because it can be harmful to the organism. What would happen if a stop codon was removed? If a stop codon is removed, the ribosome keeps adding amino acids until it reaches another stop codon. If this is close, the protein may still function, but usually the extra amino acids cause misfolding. This prevents the protein from functioning correctly and can be harmful to the organism. Effect of non-mutagen vs mutagen? Non-mutagens can trigger epigenetic markers to be turned on or off, resulting in a different expression of the phenotype without changing the genotype. Mutagens change the genotype and therefore the phenotype changes. How triplets, codons and anticodons work together? Triplets in the template strand (3 sequential nucleotides on a DNA strand) code for the codons in the mRNA. When the RNA polymerase adds the free nucleotides onto the template strand it produces codons (3 sequential nucleotides on a mRNA strand that code for amino-acids). When the mRNA goes in the translation phase the cytoplasm, the tRNA has anticodons (complementary to the codons on the mRNA strand) to ensure that the aminoacids on the tRNA are in the correct order. The chain of the amino acids produce proteins. 2 or more reasons why DNA cannot be directly transcribed into a polypeptide chain? The DNA needs to be protected in the nucleus from possible mutations that may occur in exposure in the cytoplasm and in the translation process. The tRNA that carries the amino acids is specifically shaped to be complementary to the mRNA strand. There needs to be multiple proteins produced at the same time from the same DNA strand which would not be possible as each cell only has 1 pair of chromosomes.
22 weeks ago
A podcast about The content of waves and the content of Nuclear Physics for a year 11 standard test
23 weeks ago
SatYield Live is our weekly podcast where we break down global crop yield trends using satellite data and AI. Each episode dives into the latest insights, regional highlights, and key signals from the field—helping traders, analysts, and agri-professionals stay ahead of the curve.
63 weeks ago
There have been many attempts to try and explain the intriguing depictions of animals in the caves of Europe that date from around 35,000 years ago onwards. Most of those attempts have fallen by the wayside mainly because they were incapable of being verified experimentally. This was all set to change, however, when, in 2008, Derek Hodgson wrote an article that showed how visual neuroscience and perceptual psychology could provide interesting insights into the mystery. Based on the findings of that article, a number of research groups began to apply the concepts and findings of Hodgson's article to investigating cave art by applying recent technological know-how to experimentally test the suggestions therein. The results of those experimental studies provided resounding support for Hodgson's approach. The original 2008 article is presented in this podcast not least because it was such a ground-breaking contribution to cave art research.
83 weeks ago
How does passing hard stools make period cramps worse? How does it affect the pelvic floor muscles? Does straining make the pelvic floor muscles tired and sore? Does straining make the pelvic floor muscles go into muscle guarding? How long does it take for the pelvic floor muscles to recover from straining? Treatments?
23 weeks ago
Dialogue on myths, facts, and impact of obesity in the United States.
24 weeks ago
Discussing Dr Kevin M Decker's Intersectional Consciousness Theory, with a mix of hosts: Dr Kevin Decker, James, Mark , Dr Abebe Botha, Dr van der Berg, and others.
41 month ago
Applying UV absorbance to measure tank cleanliness with Custom Sensors and Technologies PX2 UV Photometer and EZ-CAL Flow Cell
21 month ago
An alternative look at AGI - AI or AGI or Alien Consciousness with Alien Intelligence
21 month ago
Daniel Kahneman’s theory Kahneman begins by explaining the purpose of his book: to provide people with a richer vocabulary for discussing and identifying errors in judgment. He briefly traces his professional interest in the psychology of judgment and decision-making, illustrated with examples of human intuition's successes and failures. Lastly, Kahneman offers a broad overview of Thinking, Fast and Slow, starting with the functions of two complementary "systems" of cognition and describing the heuristics, or rules of thumb, these systems depend on. In the "Origins" section of the introduction, Kahneman discusses his research and his late thought partner, Amos Tversky, at length. Tversky's contributions were central to Kahneman's work and success.
61 month ago
Paper #1 🧬 ABSTRACT Over the past decade, extracellular vesicles (EVs) — tiny packages secreted by nearly all cells — have emerged as powerful players in both nanomedicine {meaning: the use of nanoscale tools or particles to diagnose, treat, or repair the body} and regenerative medicine {meaning: medical approaches that help the body heal or rebuild tissues, like bone, nerve, or heart tissue}. Researchers have discovered that EVs do more than just carry waste — they deliver proteins, RNAs {ribonucleic acids, which control gene expression}, lipids {fat-based molecules}, and other cargo between cells. This makes them important messengers in cell-to-cell communication, especially during healing or disease. The paper reviews how EVs can: Repair tissues like bone, cartilage, and muscle, Support regeneration in organs like the heart or nervous system, Deliver drugs or gene-editing tools like siRNA {short interfering RNA, used to silence specific genes}, And reduce inflammation in damaged tissues. It also explores different ways scientists are trying to engineer EVs — changing them to carry useful molecules or to better target certain cells — as well as methods to produce, purify, and use them safely in medicine. 🧠 INTRODUCTION Over the last 10 years, there's been an explosion of interest in extracellular vesicles, especially in the fields of biomedicine, drug delivery, and tissue repair. 💡 So… what makes EVs so exciting? They're like natural nanocarriers — think tiny delivery drones — that can move through the bloodstream and deliver molecular messages straight into target cells. And unlike synthetic nanoparticles or viruses, EVs are: Biocompatible {meaning: safe for the body}, Stable in circulation {meaning: they don’t break down quickly in blood}, Low in immunogenicity {meaning: they don’t usually trigger strong immune reactions}, And naturally able to cross biological barriers like the blood–brain barrier {BBB, a tightly sealed wall of cells that protects the brain from harmful substances}. Because of this, EVs are being explored for: Regrowing heart tissue after heart attacks, Healing nerve injuries, Treating osteoporosis (bone weakening), Fighting inflammatory diseases, And delivering RNA-based therapies for genetic disorders or cancer. 🔬 Types of EVs This paper mostly focuses on: Exosomes {30–150 nm vesicles made inside the cell, released by fusion of multivesicular bodies with the cell membrane}, Microvesicles {100–1,000 nm, bud directly from the membrane}, And apoptotic bodies {vesicles released during cell death}. But it’s exosomes that are getting most of the attention in regenerative medicine and nanotherapy — because of their size, stability, and natural role in cell signaling. ⚠️ Challenges Ahead Even though the potential is massive, there are still problems to solve: How do we isolate EVs reliably and purely at scale? How do we engineer them to deliver the right cargo to the right place? How do we store and administer them in real-world medical settings? That’s what this review will tackle — by summarizing major research findings from the last decade, highlighting promising clinical directions, and pointing out what still needs to be improved. 🎤 That wraps Part 1. Next up: EV biogenesis — how these little messengers are made, loaded, and released. 🎧 SECTION 2: EV Biogenesis, Cargo Loading & Isolation — Annotated Podcast Version 🧬 2.1 EV Biogenesis (How EVs Form Naturally) EVs originate from two primary cellular pathways: endosomal and plasma membrane-derived mechanisms. In the endosomal route, inward budding of the endosomal membrane forms intraluminal vesicles (ILVs) inside multivesicular bodies (MVBs). These MVBs then fuse with the plasma membrane to release ILVs as exosomes. The plasma membrane pathway, by contrast, directly buds vesicles outward into the extracellular space, forming microvesicles (MVs). These pathways are tightly regulated by proteins like ESCRT (Endosomal Sorting Complex Required for Transport) {a group of protein complexes that help sort and package cargo into vesicles} and Rab GTPases {molecular switches that help vesicles move to the right place}. 🧠 Why it matters: Understanding this biogenesis helps researchers engineer EVs to carry specific cargo — like drugs or RNA — for therapeutic delivery. 🧪 2.2 Cargo Loading Mechanisms (Natural and Artificial) Cells naturally load cargo like miRNAs, mRNAs, proteins, and lipids into EVs. However, for therapeutic use, researchers want more control. There are two general approaches: ▶️ Endogenous loading: Modifying the parent cell so that it naturally packages the desired cargo into EVs. Example: transfecting a cell to overexpress a therapeutic miRNA. ▶️ Exogenous loading: Inserting cargo after EVs are isolated. This can be done using: Electroporation {using electricity to open pores in the EV membrane} Sonication {using sound waves to push cargo in} Freeze-thaw cycles, chemical treatments, or saponin-mediated permeabilization {using a detergent-like molecule to temporarily open the EV membrane} Each has pros and cons in terms of efficiency, EV integrity, and scalability. 🧠 Why it matters: Efficient loading = more therapeutic effect. But too harsh, and the EVs fall apart. 🧲 2.3 Isolation and Purification Methods Isolating EVs from biofluids like blood or cell culture media is crucial for clinical use. The methods vary in purity, scalability, and cost. 🧱 Conventional Methods: Ultracentrifugation (UC) — the gold standard Pros: High yield Cons: Time-consuming, expensive, low purity due to co-isolated proteins Ultrafiltration Pros: Fast and scalable Cons: Filters clog easily, can damage vesicles Size Exclusion Chromatography (SEC) Pros: Gentle, preserves vesicle structure Cons: Can co-isolate similarly sized particles like lipoproteins Immunoaffinity capture Uses antibodies against EV surface markers (e.g., CD63, CD9) Pros: Highly specific Cons: Expensive, not scalable 🧪 Advanced Methods: Microfluidic isolation platforms Lab-on-a-chip devices that separate EVs based on size or surface markers Pros: Fast, requires small sample volumes Cons: Still under development for clinical-scale use Immunoaffinity-based microfluidics Combines specificity of antibodies with efficiency of microfluidics Pros: Very high purity Cons: Still experimental, costly 🧠 Why it matters: The method used affects downstream applications. For example, diagnostic tests require high purity, but drug delivery may prioritize yield. 💡 Summary of Section 2: EVs form either via endosomal (exosomes) or plasma membrane (microvesicles) pathways Cargo can be loaded naturally or artificially, each with different challenges Isolation is a huge bottleneck: no perfect method exists yet 🧬 Understanding and improving these processes is essential for EVs to move from the lab bench to the bedside. Explanation of the Exosome Clinical Trials Table Column What it Means Example from table Exosome’s application The general purpose or type of use for the exosomes in the trial — either delivering drugs, therapy, or biomarker identification. "Drug delivery" or "Therapy" or "Biomarker" Pathology The disease or condition targeted by the clinical trial. "NSCLC" (Non-small cell lung cancer) or "Psoriasis" Phase The clinical trial phase indicates how far along the trial is: 1 (safety & dosage), 2 (efficacy & side effects), 3 (large-scale testing), or NA (not applicable or unspecified). Phase 2 for NSCLC trial started in 2010. Start year The year the clinical trial began. 2010 for the NSCLC trial. Source of exosome Where the exosomes used in the trial were originally harvested or derived from. Could be a type of cell, tissue, or even plants. "Dendritic cells," "MSCs" (mesenchymal stem cells), "Plant (ginger)" Sponsor The institution or company funding or conducting the clinical trial. "Gustave Roussy," "University of Louisville," "ILIAS Biologics Inc." Clinical trial number The unique identifier (NCT number) assigned to the trial in clinical registries (like ClinicalTrials.gov), so you can look up details. NCT01159288 for the NSCLC trial. How to interpret this? If you see "Drug delivery" under application, the exosomes are being tested to carry and release drugs to treat diseases, for example, delivering chemotherapy drugs directly to cancer cells. If you see "Therapy", it means the exosomes themselves or what they carry are being tested as the main treatment — like using stem cell-derived exosomes to reduce inflammation. Biomarker trials are investigating if exosomes can help detect or diagnose diseases, like using exosomes found in blood to identify cancer early. The Phase tells you how mature the trial is: Phase 1 = Safety check on a small number of patients Phase 2 = Looks at effectiveness and side effects in a bigger group Phase 3 = Large-scale confirmation of results before approval NA = Might be early research or observational studies without these phases. The Source of exosome is important because exosomes carry molecular information from their origin cells, influencing their therapeutic potential. For example: Dendritic cells exosomes may stimulate immune responses. MSCs (mesenchymal stem cells) exosomes often have regenerative and anti-inflammatory effects. Plant-derived exosomes (like from ginger or grapes) are being explored for oral delivery and anti-inflammatory properties. The Sponsor tells you who is responsible for the trial, which can be a hospital, university, or biotech company. The Clinical trial number lets researchers or curious people find detailed info about the trial on official databases. Example — First Row Explained: | Drug delivery | NSCLC | 2 | 2010 | Dendritic cells | Gustave Roussy, Cancer Campus, Grand Paris | NCT01159288 | Exosomes are used to deliver drugs to treat non-small cell lung cancer (NSCLC). The trial is in phase 2 (testing efficacy and side effects). It started in 2010. The exosomes are derived from dendritic cells (immune cells). Sponsored by the Gustave Roussy Cancer Campus in France. You can look it up with the clinical trial number NCT01159288. Exosomes in Nanomedicine & Drug Delivery: General Exosomes are natural nanovesicles secreted by cells that play roles in cell communication, disease progression, and therapy. They have excellent biocompatibility, stability, and can cross biological barriers like the blood-brain barrier (BBB). These properties make exosomes attractive for: Therapeutic delivery vehicles Disease biomarkers Cell-free vaccines and immune modulators 3. Examples of Exosome Drug Delivery Applications by Organ/System 3.1 Brain Disorders The BBB restricts delivery of almost all large biologics and 98% of small molecule drugs, so exosomes’ natural ability to cross BBB is crucial. Exosomes can deliver therapeutic agents to brain tumors (e.g. glioblastoma), neurodegenerative diseases (Alzheimer’s, Parkinson’s, Huntington’s), and CNS infections. Example cargoes: miRNAs (e.g. antisense miRNA-21 for glioblastoma) Chemotherapy drugs (e.g. doxorubicin) Catalase mRNA to reduce neuroinflammation in Parkinson’s siRNA for gene silencing in Huntington’s Loading techniques include pre-isolation transfection (genetically engineering source cells) and post-isolation active loading (sonication, electroporation). Targeting ligands like transferrin help exosomes home to tumors or specific brain regions. 3.2 Lung Disorders Exosomal miRNAs regulate drug resistance, angiogenesis, and cancer cell proliferation in lung cancer. Exosomes from breast cancer cells can specifically interact with lung cancer cells via membrane proteins (e.g., surfactant protein C, integrin 4). Exosomes from cow milk loaded with siRNA against KRAS (a major oncogene) reduce tumor growth in lung cancer models. They also show promise in treating other lung diseases: inflammation, injury, fibrosis, asthma. 3.3 Liver Disorders Hepatocellular carcinoma (HCC) is a leading cause of cancer death; exosomes carrying miRNA-122 can increase chemotherapy sensitivity and inhibit tumor growth. Exosomes loaded with CRISPR-Cas9 ribonucleoprotein complexes can deliver gene editing machinery to liver cells for gene therapy. Exosomes mediate immune responses and viral propagation in hepatitis infections; they influence inflammation and immune evasion. 3.4 Other Cancers & Diseases Doxorubicin-loaded exosomes improve efficacy and reduce toxicity compared to free drug in breast, ovarian, colon, pancreatic, prostate, and osteosarcoma cancers. Other drugs like paclitaxel, curcumin, and cisplatin have been loaded into exosomes for targeted delivery. Exosomes can be engineered for tissue-specific targeting, improving personalized medicine potential. Raw milk exosomes may help deliver antioxidant and anti-inflammatory anthocyanidins effectively. 4. Exosome Advantages Natural biocompatibility and low immunogenicity Ability to cross biological barriers like BBB Specific targeting ability by modifying surface proteins High stability and capacity to carry diverse cargoes (RNAs, drugs, proteins) Potential for personalized and precision therapies 5. Summary of Loading & Characterization Techniques Loading Technique Description Pre-isolation Transfection Engineering source cells to express/load cargo before EV release Post-isolation Sonication Physically loading cargo after isolation by sonication Electroporation Electrical pulses to open EV membranes for cargo loading Direct Transfection Chemical/physical transfection of EVs with cargo Passive Incubation Simple incubation allowing cargo diffusion into EVs Characterization methods include: Transmission Electron Microscopy (TEM) Nanoparticle Tracking Analysis (NTA) Dynamic Light Scattering (DLS) Western Blot (WB) RNA sequencing (RNA-seq) Proteomics Flow cytometry (FCM) Scanning Electron Microscopy (SEM) Atomic Force Microscopy (AFM) ELISA 6. Important Concepts Blood-Brain Barrier (BBB): a selective barrier preventing most drugs from entering the brain. Exosomes can cross it, making them promising for brain therapies. MicroRNAs (miRNAs): small noncoding RNAs regulating gene expression, often used as therapeutic cargo or biomarkers. Mesenchymal Stem Cells (MSCs): stem cells commonly used as a source for therapeutic exosomes. CRISPR-Cas9: gene-editing technology delivered via exosomes to target specific genes. 🧬 SECTION 4: Exosomes in Cancer Immunotherapy Exosomes are being explored as powerful immunotherapeutic agents in cancer. That means they might help train the immune system to recognize and attack cancer cells. One reason exosomes are great for this is because they can carry tumor antigens — the little “flags” on cancer cells that identify them as targets. There are two major ways exosomes can be used in cancer immunotherapy: 4.1. As Cell-Free Cancer Vaccines Some studies have used tumor-derived exosomes (TEXs) — which are just exosomes coming from cancer cells — as vaccines. These TEXs carry tumor-specific proteins and can stimulate immune cells, especially cytotoxic T lymphocytes (CTLs) {meaning: killer T cells that destroy infected or cancerous cells}. For example, dendritic cells (DCs) {meaning: immune system “scouts” that process and present antigens} loaded with tumor-derived exosomes have been shown to stimulate antitumor immune responses in mice and human trials. Even more advanced: instead of loading dendritic cells manually, some researchers are now directly injecting TEXs to stimulate T-cell responses. 💡 This shows that exosomes could someday replace traditional cancer vaccines — doing it more naturally and safely. 4.2. As Immune Modulators Exosomes can also modulate or influence the immune system — in good or bad ways. On one hand, immune cell-derived exosomes (like from NK cells or T cells) can kill tumor cells directly or activate more immune responses. On the other hand, some tumor-derived exosomes might suppress immunity — like making T cells tired or reducing antigen presentation. So scientists are exploring engineered exosomes to only promote positive effects and block the bad ones. 🎯 SECTION 5: Exosome Targeting Strategies in Cancer Therapy If you're going to treat cancer with exosomes, you need to make sure they deliver the right cargo (like siRNA, miRNA, or drugs) to the right tissue — not everywhere. This section is about how we can engineer that “targeting.” There are two big strategies here: 5.1. Natural Targeting (Inherent Tropism) Exosomes sometimes naturally go to certain tissues based on where they came from. For example: Exosomes from brain cells often cross the blood-brain barrier (BBB) {meaning: the protective lining that blocks many drugs from entering the brain}. Tumor-derived exosomes tend to “home in” on tumors — maybe because of the shared surface markers. This natural targeting is called tropism {meaning: natural attraction toward a certain tissue or environment}. 5.2. Engineered Targeting Scientists are now customizing exosomes by decorating their surface with targeting ligands {meaning: molecules that bind to specific receptors on target cells}. Example: Attaching RGD peptides {meaning: a short protein sequence that binds to integrins on tumor blood vessels} so that the exosome delivers its payload only to tumors. Another method: fusing transferrin, which binds to transferrin receptors overexpressed in cancer cells, directly to the exosome membrane. ⚒️ Methods for engineering this include: Genetic fusion (adding coding sequences for targeting proteins) Chemical conjugation (using click chemistry to attach molecules to the membrane) This allows for precision targeting and could be super useful in your EXODEC design. 🔍 SECTION 6: Exosomes as Biomarkers in Cancer Exosomes are also rich diagnostic tools because their content reflects the condition of the parent cells. That means a simple blood or urine test could reveal cancer signs way earlier than current methods. Key highlights: 6.1. Cargo Mirrors Cancer Progression Exosomes from cancer patients often contain: Specific miRNAs {meaning: small RNA molecules that regulate genes and are often messed up in cancer} Mutant proteins or oncogenes (like mutant KRAS, EGFRvIII, or HER2) Long noncoding RNAs (lncRNAs) or even DNA fragments Because exosomes can cross barriers and float in bodily fluids, this makes them ideal for liquid biopsy {meaning: a simple blood test that can detect cancer without a tissue sample}. 6.2. Diagnostic Panels Are Emerging Scientists are building exosome-based biomarker panels to diagnose or track cancer types like: Lung cancer (e.g., exosomal miR-21 and miR-210) Pancreatic cancer (e.g., GPC1 protein in exosomes) Glioblastoma (e.g., EGFRvIII-containing exosomes) Many of these panels are non-invasive, reproducible, and may someday be part of your regular checkup. 6.3. Challenges and Next Steps BUT — to use exosomes as official clinical biomarkers, we need: Standardized isolation and purification Better understanding of which exosome subtypes are informative Large-scale clinical studies This is where your science fair project EXODEC could tie in beautifully — maybe by helping improve targeting, isolation, or disease-specific detection. ✅ TL;DR Summary: Application Area Use of Exosomes Key Techniques / Challenges Cancer Immunotherapy Vaccine-like role, stimulate T-cells, modulate immune response Need to engineer away immune suppression Targeted Delivery Deliver drugs/siRNA/miRNA to tumors Use natural tropism or attach ligands (like RGD, transferrin) Biomarker Discovery Detect miRNAs, proteins, DNA in fluids Build reliable, standardized diagnostic panels What the Table Shows The table lists multiple disorders or target tissues and connects each to: Source of the exosomes: Where the exosomes come from, e.g., mesenchymal stem cells (MSCs), cardiac cells, adipose-derived stem cells (ASCs), etc. Aim of using exosomes: The therapeutic goal, e.g., improving cardiac function, promoting nerve regeneration, reducing inflammation, stimulating bone growth, etc. Regenerative medicine methodology: The biological mechanism or pathway through which exosomes act, such as delivering specific microRNAs (miRNAs), proteins, or signaling molecules; activating certain molecular pathways; reducing apoptosis (cell death); promoting angiogenesis (new blood vessel formation); etc. Experimental context: Whether the study was done in vitro (in cell culture), in vivo (in living organisms, often animal models), or ex vivo (in isolated tissues). References: The numbers refer to original studies, showing this is a literature review or meta-analysis. Key Themes & Why It Matters 1. Exosomes mimic stem cell therapies but are safer and easier to use Exosomes carry the beneficial factors secreted by stem cells without needing to transplant the whole cell, avoiding immune rejection and other risks. They are more stable and easier to store and deliver. 2. Wide range of tissues targeted Heart: exosomes promote cardiac repair by carrying miRNAs and proteins that enhance heart muscle cell survival, reduce fibrosis, and stimulate blood vessel growth. Central & Peripheral Nervous Systems: they help nerve regeneration, reduce inflammation, and prevent neural cell death, crucial for stroke or nerve injury recovery. Skin: exosomes aid wound healing, reduce inflammation, combat aging/photoaging, and improve skin hydration. Muscle: they promote muscle regeneration, increase muscle cell proliferation, and reduce scarring. Liver: exosomes help regeneration after injury by activating regenerative signaling pathways. Blood vessels: promote angiogenesis by regulating key growth factors and genes. Cartilage: aid cartilage repair by promoting cell proliferation and reducing inflammation. Ovary: used to treat premature ovarian insufficiency by preventing cell death and promoting cell growth through various signaling pathways. Bone: enhance bone formation and healing by regulating osteogenic (bone-forming) factors and pathways. 3. Molecular mechanisms Many entries mention specific miRNAs (small RNA molecules that regulate gene expression), signaling pathways (like PI3K/Akt, Wnt/β-catenin, MAPK, etc.), or proteins (e.g., heat shock proteins, growth factors) that are transferred or influenced by exosomes. These mechanisms explain how exosomes exert their therapeutic effects at the cellular level. 4. Research stages Some studies are in vitro (cell cultures), some in vivo (animal models), and some are a mix, indicating how far along each approach is in development. Summary of Why This Table is Important Exosomes are emerging as powerful cell-free therapies that can promote healing, regeneration, and functional recovery in many tissues by delivering bioactive molecules. They can target complex diseases and injuries by modulating inflammation, cell death, tissue remodeling, and regeneration. The table shows how exosomes derived from different stem cells or tissues are being explored extensively across regenerative medicine, making them versatile tools with clinical promise. Understanding the specific miRNAs and pathways involved can help design more effective exosome-based treatments tailored for particular organs or diseases. 7.1 Myocardial (Heart) Regeneration Context: After heart damage (e.g., heart attack), regenerating heart muscle (myocardium) is tough because heart cells don’t divide much naturally. Stem cells like mesenchymal stem cells (MSCs), cardiac stem cells, embryonic stem cells, etc., release exosomes — tiny vesicles (50-100 nm) carrying proteins, RNA, and signaling molecules. These exosomes can reduce heart damage by: Lowering oxidative stress (damaging reactive oxygen species), Increasing energy molecule ATP in cells, Activating protective cell pathways (like PI3K/Akt), Protecting cells from programmed death (apoptosis), Promoting new blood vessel growth (angiogenesis), Reducing inflammation and fibrosis (scar tissue). Example: MSC-derived exosomes reduced infarct size in mice and rats. Different exosome sources matter — e.g., diabetic rat heart cell exosomes inhibit blood vessel growth due to specific microRNAs they carry (miR-320 up, miR-126 down). Some researchers pre-treat MSCs (with atorvastatin or GATA-4 gene) to produce exosomes with stronger protective effects. Targeting exosomes specifically to damaged heart tissue is being done by attaching homing peptides to exosomes, improving delivery and therapeutic effect. Why important: These findings show exosomes could be a minimally invasive, cell-free therapy for heart repair, overcoming challenges of stem cell therapy. 7.2 Neuronal (Nerve) Regeneration Context: Nerves in the brain, spinal cord, and peripheral nerves regenerate poorly after injury. Exosomes from nervous system cells or MSCs can promote nerve regeneration by transferring beneficial miRNAs (small regulatory RNA molecules) and proteins. Examples: Serum exosomal miR-9 and miR-124 are promising stroke biomarkers. MSC-derived exosomes with miR-124 improve neuron growth after traumatic brain injury by inhibiting harmful inflammatory pathways (like TLR4). Exosomes transfer miR-133b to neural cells, enhancing recovery after stroke. Exosomes from adipose-derived stem cells (ADSCs) promote peripheral nerve repair by supporting Schwann cells (cells that form myelin sheath) and reducing apoptosis. Exosomes from endothelial cells carrying miR-199-5p activate pathways promoting Schwann cell repair. Some exosomes come from Schwann cells themselves and support nerve regeneration. Targeting proteins inside exosomes (like Argonaute-2) shows miRNA content is critical for their regenerative effect. Combining exosomes with 3D scaffolds may further boost nerve repair. Why important: Exosome therapies could enable recovery from nerve injuries, stroke, and neurodegenerative diseases without complex cell transplantation. 7.3 Cutaneous (Skin) Regeneration Exosomes from stem cells, bacteria, and plants can improve skin healing, rejuvenation, and protection from UV damage. They act by interacting with skin cells and extracellular matrix (the structural network of skin), influencing: Activation of cell growth pathways (PI3K/AKT, Wnt/β-catenin, TGF-β), Regulating collagen production (important for skin strength and elasticity), Modulating inflammation by downregulating cytokines and NF-κB pathway, Accelerating wound closure, Reversing UV-induced damage and hyperpigmentation, Increasing skin hydration and reducing enzymes that break down collagen. Collagen regulation varies by wound healing phase (early vs. late). Why important: This suggests exosomes could be used as therapies for wound healing, anti-aging skin treatments, and protection against sun damage. 7.4 Muscle Regeneration Exosomes from adipose-derived stem cells (ADSCs), MSCs, and other muscle-related cells promote muscle repair by: Enhancing muscle cell proliferation and differentiation (growth and maturation), Increasing expression of key muscle genes like MYOG (myogenin) and MYOD, Inhibiting muscle atrophy (wasting), Modulating growth factors and anti-apoptotic miRNAs (miR-21, miR-1, miR-133, miR-206, etc.). Non-stem cell exosomes from macrophages or muscle cells (like C2C12) also promote muscle repair via gene regulation. Mechanical strain on muscle cells can make their exosomes more effective for repair. Why important: Exosome therapies could improve healing in muscle injuries or degenerative muscle diseases. 7.5 Vascular (Blood Vessel) Regeneration Exosomes from endothelial cells (lining blood vessels) and progenitor cells promote blood vessel growth by delivering miRNAs that: Increase angiogenic factors like VEGF, eNOS, HIF-1α, Enhance endothelial cell proliferation, migration, and new blood vessel formation. Exosomes from MSCs cultured on special materials or with growth factor supplements (like PDGF) have enhanced angiogenic potential. Hypoxia (low oxygen) stimulates cells to release exosomes with stronger angiogenic effects—tumor cells under hypoxia produce exosomes that promote blood vessel growth, aiding tumor progression. Overexpression of miR-21 in exosomes increases pro-angiogenic proteins and decreases inhibitors like PTEN. Why important: These findings highlight exosomes’ role in therapeutic vascular regeneration (e.g., healing ischemic tissues) but also their potential in tumor angiogenesis (which may be a treatment target). Summary of Why This Matters: Exosomes are natural nanoscale messengers released by cells, carrying miRNAs, proteins, and signaling molecules. They can regenerate damaged tissues in heart, nerve, skin, muscle, and blood vessels by modulating cellular processes like survival, growth, inflammation, and angiogenesis. Their small size and natural origin make them promising cell-free therapeutic agents avoiding risks of whole-cell transplants. Understanding the source and molecular cargo of exosomes is key to harnessing their benefits safely and effectively. Advances include targeting exosomes to injured tissues and engineering their content to boost therapeutic effects. 7.6 Chondral (Cartilage) Regeneration Background: Cartilage damage (e.g., in osteoarthritis) is hard to repair because cartilage has limited self-healing. Exosomes from MSCs (mesenchymal stem cells) show promise to promote cartilage regeneration by: Increasing cartilage cell proliferation and survival, Modulating immune responses (increasing regenerative M2 macrophages, reducing inflammatory cytokines like IL-1β and TNF-α), Activating key signaling pathways (AKT, ERK, Wnt), Promoting cartilage matrix production. Different MSC sources (bone marrow, embryonic, fat-derived, synovial membrane) and chondrocyte-derived exosomes vary in effectiveness. Pretreating MSCs with molecules like kartogenin enhances their exosomes’ ability to induce cartilage formation. Overexpression of specific miRNAs (e.g., miR-140-5p, miR-199a-3p) in MSC-derived exosomes improves cartilage repair. Induced pluripotent stem cell (iPSC)-derived MSC exosomes seem even more potent for cartilage regeneration. Why important: These findings support exosome-based therapies for osteoarthritis and cartilage injuries, potentially offering alternatives to joint replacement or invasive surgery. 7.7 Hepatic (Liver) Regeneration Background: Liver can regenerate but can be overwhelmed by injury or disease. Exosomes from healthy hepatocytes transfer enzymes like sphingosine kinase (SK2) to promote liver cell proliferation after injury. MSC-derived exosomes promote liver regeneration and reduce fibrosis by: Stimulating hepatocyte proliferation, Activating antioxidant defenses (e.g., glutathione peroxidase 1), Modulating signaling pathways like Wnt/β-catenin and AKT/mTOR, Carrying circular RNAs (circ-RBM23) that regulate miRNAs involved in proliferation. Placenta MSC exosomes also promote regeneration via Wnt signaling and proteins like C-reactive protein. Exosomes from liver progenitor-like cells improve regeneration by modulating the FoxO1/Akt/GSK3β/β-catenin signaling axis. Why important: Exosomes could become cell-free therapies to treat acute liver injury, chronic liver disease, or support liver surgery recovery. 7.8 Ovary Regeneration Context: Premature ovarian insufficiency (POI) causes infertility; current treatments are limited. Stem cell–derived exosomes show therapeutic potential by: Preventing apoptosis (programmed cell death) of ovarian granulosa cells via multiple pathways (e.g., YAF2/PDCD5/p53, PI3K/AKT/mTOR), Delivering miRNAs (e.g., miR-369-3p, miR-126-3p, miR-17-5p, miR-144-5p, miR-664-5p) that regulate genes to prevent cell death, Enhancing extracellular matrix proteins (collagen IV, fibronectin, laminin) important for ovarian structure, Increasing hormone levels (estradiol (E2), anti-Müllerian hormone (AMH)) and reducing follicle-stimulating hormone (FSH), Increasing follicle number and corpus luteum formation, Ultimately improving fertility and birth rates in animal models. However, effects may not last long-term; more studies are needed before clinical use. Why important: Exosome therapy could become a novel, less invasive option for women with POI or other ovarian dysfunctions. 7.9 Skeletal (Bone) Regeneration Context: Bone injuries or diseases require effective regeneration to restore structure and function. MSC- and ADSC-derived exosomes promote bone regeneration by: Increasing osteogenic genes/proteins such as RUNX2 (bone formation regulator), ALP (enzyme marker for bone growth), COL1A1 (type I collagen), Enhancing angiogenic factors (VEGF, ANG1, ANG2) to support blood supply, Modulating miRNAs (e.g., upregulating miR-146a-5p, miR-503-5p; downregulating miR-133a-3p) involved in bone growth and remodeling, Activating signaling pathways like PI3K/Akt and MAPK important for cell proliferation and differentiation. Genetic modification of MSCs (e.g., overexpressing miR-21, HIF-α) further boosts the bone healing properties of their exosomes. Targeted delivery to bone tissue has been improved by attaching specific molecules (aptamers) to exosomes. Aging reduces MSC exosome regenerative capacity due to different miRNA content. iPSC-derived MSC exosomes also promote bone healing effectively. Exosomes can reduce apoptosis (cell death) in bone cells and promote vascularization critical for bone repair. Why important: Exosome therapies could offer advanced treatments for fractures, osteoporosis, and other skeletal conditions, improving healing speed and quality. Overall Key Points: Across these tissues, MSC-derived exosomes are powerful mediators of regeneration due to their cargo of proteins, miRNAs, and signaling molecules. They promote healing by enhancing cell survival, proliferation, differentiation, and reducing inflammation. Preconditioning or genetic modification of MSCs can improve exosome therapeutic effects. Different sources of exosomes (bone marrow, adipose tissue, iPSCs, placenta, chondrocytes) have different strengths. Research is advancing toward cell-free therapies that avoid risks of stem cell transplantation but still harness regenerative potential. 🎯 Section 8: Limitations and Challenges While exosomes are very promising, there are several important challenges holding them back from widespread use in clinical settings: 1. Difficult Isolation & Detection Ultracentrifugation (the standard method) is slow, expensive, and not very precise, which can reduce the exosomes' biological effectiveness. Commercial kits exist, but they're too costly and mostly limited to lab research. Researchers are exploring better techniques like: Magnetic nanoparticles fused to transferrin (e.g., Qi et al.) for easy targeting and simpler isolation. 2. Heterogeneity of EVs (Extracellular Vesicles) EVs (including exosomes) are not a uniform group—there are different subtypes with different biological roles. Current tech isn’t yet able to fully distinguish or isolate these subpopulations, making research and therapy more complex. 3. New Nano-Based Detection/Isolation Technologies These are cutting-edge and aim to be cheaper, faster, and more accurate: Nano-DLD: Isolates super small exosomes (20–100 nm), but still hard to design/manufacture for real-world use. RPS (Resistive Pulse Sensing): Measures shape, size, and charge at the single-particle level. SPR-based nanosensors: Detect exosomes via surface interactions—fast, scalable, and doesn’t require labeling. 4. Targeting Specificity and Circulation Time Exosomes often get cleared too quickly from the bloodstream and may not target the right tissue. Strategies to improve this include: Surface modifications (e.g., adding peptides or ligands for targeting specific cells). PEGylation (adding PEG polymers) extends circulation time from 10 min → 60+ min. Exosome-liposome hybrids: Help with stability, immune evasion, and cellular uptake. 5. Limited Understanding of Their Mechanisms Scientists still don’t fully know how exosomes actually cause tissue regeneration or how they interact with cells. It's unclear how they: Enter cells Deliver drugs Influence cancer progression or suppression 6. Storage and Stability Exosomes don’t store well long-term. Freezing, freeze-drying, and spray-drying are commonly used, but they damage activity or structure. Better storage methods are urgently needed. 7. Challenges in Drug Loading It's hard to measure and optimize how much drug gets loaded into an exosome or how efficiently it carries it. Many studies don’t even report the ratio of exosome to drug. ✅ Section 9: Concluding Remarks This section wraps up everything by summarizing the potential of exosomes and the work still needed: Why exosomes matter: They’re great messengers between cells. They cross biological barriers better than synthetic nanovesicles. They’re useful in: Drug delivery Diagnostics (biomarkers) Tissue regeneration Cancer immunotherapy and vaccine development Main hurdles: Mass production is hard because we still rely on slow, inefficient isolation methods. Purity is critical—clinical-grade exosomes must be free from contaminants and unused drug molecules. Molecular mechanisms and signaling pathways of exosomes are still not fully known. Better technologies are needed to: Identify exosomes Understand their targets Make sure they work effectively and safely The way forward: Exosomes that follow Good Manufacturing Practices (GMP) can be used in human trials. Collaboration across disciplines (doctors, biologists, engineers, and data scientists) is essential to make exosome therapy a real clinical option.
21 month ago
The impact of physical and environmental geography on the location of human settlement as well as the impact that geography has on climate.
21 month ago
Here, there are several short podcasts, around 5-minutes, to help you with the study questions in the 'Unit 2: Animal Biology Padlet and to help with your exam revision :)
21 month ago
Going from almost extinct to a household pet, we take you through the story of the Gecko.
91 month ago
Austin and Hollie.AI discuss hot topics and edge papers in cardiology.
72 months ago
A podcast of the knowledge organisers of the Science Curriculum at Masefield.
22 months ago
That Time I Saw Sasquatch: Podcast Summary Overview That Time I Saw Sasquatch is a podcast that brings to light the often-overlooked stories of women who have encountered Bigfoot. Focusing exclusively on female witnesses, the podcast weaves together firsthand accounts, interviews with researchers, and discussions about the unique perspectives women bring to the world of cryptozoology. Episode Highlights Childhood and Lifelong Encounters Mrs. W. (Kalamazoo, Michigan): Shares her story of physically running into a towering Sasquatch as a child, describing its gentle yet powerful presence. Years later, she recounts a second encounter near her home, emphasizing the emotional impact and sense of recognition she felt. Rural and Remote Sightings Jacqueline Lange (Manitoba, Canada): Details a chilling nighttime encounter on a horse ranch, where a massive creature growled and leapt away, witnessed by both her and a coworker. Virginia Louise (Swanson) (San Diego County, California): A retired veterinarian, Virginia discusses her multiple Bigfoot sightings in the California backcountry, highlighting the credibility and detail in her recollections. Roadside and Unexpected Encounters Anonymous Roadside Witness (USA, 2001): Describes seeing a tall, barrel-chested figure with distinctly female features standing by the road. The witness provides a vivid description of the creature’s appearance, including its facial features and movement. Women as Researchers and Repeat Witnesses Becky Cook (Idaho): As both a journalist and an experiencer, Becky recounts her own sightings and shares stories from dozens of other women she has interviewed across Idaho. Barbara Shoop (Washington): Discusses ongoing activity on her property, including rock-throwing, vocalizations, and direct visual encounters. Barbara’s story highlights the persistence and curiosity that women bring to Bigfoot research. Themes and Insights Diversity of Experiences: The podcast showcases a wide range of encounters, from fleeting roadside glimpses to repeated, close-up interactions in rural areas. Emotional Impact: Many women describe not just fear or shock, but also curiosity, empathy, and a sense of connection during their encounters. Community and Validation: The podcast emphasizes the importance of sharing stories in a supportive environment, helping women feel validated and less isolated in their experiences. Female Researchers: Episodes feature women who are both witnesses and investigators, illustrating their growing role in the Bigfoot research community. Sample Table: Featured Sightings Name Date(s) Location Description Highlights Mrs. W. 1970s, ~1980s Kalamazoo, MI, USA Childhood and adult encounters; physical contact and visual sighting Jacqueline Lange Early 1980s Manitoba, Canada Tall creature, aggressive growling, witnessed by two people Virginia Louise (Swanson) 1981 San Diego County, CA, USA Multiple encounters, documented in her writing Anonymous Woman ~Oct 2001 USA (location not specified) 8–9 ft tall, female features, close roadside sighting Becky Cook Ongoing Idaho, USA Researcher and witness, 60+ reports collected Barbara Shoop 2014, ongoing Washington State, USA Multiple encounters, rock-throwing, bipedal and quadrupedal movement Conclusion That Time I Saw Sasquatch offers a platform for women to share their Bigfoot experiences, providing depth, detail, and a sense of community often missing from mainstream cryptozoology discussions. The podcast highlights the credibility and diversity of female witnesses, challenging stereotypes and enriching the broader conversation about the Sasquatch phenomenon.
22 months ago
This podcast features AI hosts in conversational debates on ethical issues like bias in generative AI and privacy in quantum computing. It explores emerging 2025 trends such as multimodal AI, sustainable tech, and biotechnology innovations.
22 months ago
Australia faces one of the highest obesity rates globally, linked to rising type 2 diabetes. Visceral fat, hormonal imbalance, poor diet, stress, and inactivity drive metabolic disruption. Evidence-based lifestyle changes and GLP-1 medications offer promising interventions.
22 months ago
General biology 1, all about cells,parts function , eukaryotic and prokaryotic
22 months ago
Hold onto your hormones, folks! Dr. Richard Nkwenti’s The Estrogen Equation isn’t your grandma’s biology lesson. Forget everything you thought you knew about estrogen! This powerhouse hormone isn’t just about periods and pregnancy—it’s the body’s ultimate multitasker, secretly running the show on metabolism, immunity, and even cancer risk. Dr. Nkwenti flips the script, revealing estrogen as a metabolic maestro (shaping weight, blood sugar, and energy), an immune conductor (boosting defenses but sometimes triggering autoimmunity), and a cancer risk modulator (yes, it’s complicated!). 🔬 The game-changer? Precision Hormone Modulation! No more one-size-fits-all solutions. Dr. Nkwenti’s vision combines cutting-edge tech (think AI and genomics) with lifestyle magic. Want to hack your hormones? Load up on phytoestrogen-rich foods (soy, flaxseeds!), sweat smarter with exercise, and ditch endocrine disruptors in plastics. The book serves up science-backed strategies to balance estrogen naturally—because who doesn’t want better metabolism, fewer infections, and lower cancer risk? 💡 But here’s the kicker: Estrogen is a double-edged sword! Too little? Hello, inflammation and weight gain. Too much? Autoimmunity alert. Dr. Nkwenti’s solution? Personalize everything! Your genes, diet, and environment hold the keys to your hormonal sweet spot. The future? Tailored therapies that tweak estrogen like a pro DJ mixing tracks—optimizing health span, resilience, and turning aging myths on their head. ✨ Bottom line: This book is your backstage pass to hormonal intelligence. Dr. Nkwenti makes science fun, empowering you to rewrite your health equation. Ready to rock your biology? Tune in—your hormones will thank you!" 🌟
62 months ago
Want to discover more? Explore all podcasts on Jellypod