A team of researchers at Massachusetts General Hospital has developed a new way to culture liver cells for drug toxicity screening, using a high-oxygen environment and serum-free medium. This method significantly improves the function of cultured liver cells, enabling them to predict the clearance rates of drugs with high accuracy.
Researchers found that mice lacking protein S suffered massive blood clots and defective blood vessels, highlighting the protein's dual role in coagulation and inflammation. Protein S also binds to receptors that regulate immune responses, suggesting new targets for gene therapy.
Researchers have discovered a potential therapeutic agent for treating hepatic fibrosis, a scarring condition that impairs liver function and can lead to organ failure. The CCN2 hammerhead ribozyme shows promise in reducing collagen production and cell proliferation, offering new hope for millions affected by liver fibrosis.
A team of researchers has identified XIAP as the critical factor determining which cell death pathway is followed to culminate in a cell's death. This finding has implications for cancer patients with underlying liver conditions who are being treated with IAP inhibitors.
The Gene Expression Atlas collates data from over 1000 studies, providing insights into gene function and development of new drugs. The resource allows users to query gene expression under various conditions, enabling researchers to identify key genes in specific diseases.
Researchers at Baylor College of Medicine have developed a system to target therapeutic genes to nerves in the dorsal root ganglion (DRG), showing dramatic efficiency in gene delivery compared to nontargeted adenoviruses. In mice lacking the Hexb gene, administration of DRG-targeted helper-dependent adenoviruses carrying the Hexb gene ...
Research by B.L. McVicker et al. found that reactive oxygen species are involved in ethanol-mediated cell death, but their presence is not solely responsible for apoptosis. The study also revealed that sustained cellular glutathione levels play a crucial role in this process.
Death receptors, which eliminate unwanted cells, may also be used to strengthen cells against illnesses. Researchers can develop new therapeutics that target these receptors to treat various diseases.
A new study found that transplanted liver cells from older donors work equally well in both young and old recipients, but have lower proliferation rates due to lower growth factor levels. The research suggests that injecting the growth factor IGF1 into older rats may increase hepatocyte cell proliferation.
A team of researchers from Massachusetts General Hospital has found evidence of cell-to-cell communication by amino acids, leading to faster recovery of hepatocyte activity. The study reveals that proline, a building block of collagen, plays a key role in this process.
Researchers propose using intrahepatic transplantation of hepatic oval cells to treat fulminant hepatic failure. Studies show that this approach improves liver function and increases survival rates in rats.
Research reveals cathepsin B's role in hepatocyte apoptosis and liver injury in fulminant hepatic failure. Inhibition of cathepsin B attenuates apoptosis and liver damage.
Researchers at Baylor College of Medicine have made a significant discovery in the fight against type 1 diabetes, using adult stem cells to induce liver cells to produce insulin. The study found that a specific gene called neurogenin3 is critical for this process.
Researchers at the University of Alberta discovered that hepatitis C virus causes direct damage to liver cells and leads to inflammation. This finding sheds new light on the virus and provides potential targets for therapy.
Researchers at Rockefeller University identified a human protein, occludin, that makes mouse cells susceptible to the hepatitis C virus. This discovery provides a clear foundation for developing an animal model and tailored treatments for the disease.
Researchers discovered that long stretches of DNA containing many genes are silenced in cells as they mature, rather than individual genes. This epigenetic modification, called LOCKS, plays a crucial role in cell differentiation and development.
A novel protein marker identifies rare adult liver stem cells whose ability to regenerate injured liver tissue has the potential for cell-replacement therapy. The finding offers significant implications for treating chronic liver disease in the future.
Researchers found that transplanted bone marrow mononuclear cells reduced liver fibrosis and improved albumin expression in mice infected with Schistosoma mansoni. The study suggests the potential of cell-based therapies for patients with chronic liver diseases.
Researchers explored the effects of ethanol on IGF-I system and JNK1/2 activity, revealing its role in liver damage. Ethanol exposure altered p-JNK1/2 activity, IGF-I system, and cell viability in hepatocytes.
Research found that apoptosis in liver cells leads to decreased total and free choline compound concentrations, but synthetical choline remains unchanged, providing insight into the puzzle of early-stage apoptosis changes.
Researchers found taurine to significantly decrease organelle injury scores and improve hepatocyte recovery in experimental liver fibrosis. Taurine's ultrastructural changes were also correlated with light microscopy findings, suggesting its potential as an antioxidant drug.
Researchers have determined the 3D structure of UHRF1's Set and Ring Associated domain, crucial for ensuring accurate epigenetic code copying. This breakthrough facilitates a better understanding of epigenetics and its role in cancer development.
Researchers at Cold Spring Harbor Laboratory found that senescent liver cells can orchestrate a sequence of events that limit fibrosis, a natural response to acute damage. This discovery suggests a new therapeutic approach for human patients with precursors of serious liver diseases.
A University of California, San Diego researcher has created a novel culture system that models HCV infection in human liver cells, providing a realistic environment to test new treatments. This breakthrough enables the screening of possible therapies for HCV, which affects approximately 170 million people worldwide.
Scientists have created human liver cells from embryonic stem cells, enabling drug toxicity studies and potential treatments for liver diseases. Researchers also found that innate immunity influences the response to treatment for chronic hepatitis C and discovered a link between urinary tract infections and primary biliary cirrhosis.
Researchers have developed a radial flow bioreactor system using embryonic porcine liver cells and HGF, showing potential for a fully functional artificial liver. The system promotes cell differentiation and survival, creating organoids with bile duct-like structures.
IGF-I exerts mitochondrial protection in experimental cirrhosis, reducing caspase activation and increasing ATP production. IGF-I supplementation shows beneficial effects on liver function and fibrosis in animal models.
Researchers at Massachusetts General Hospital have discovered that grapefruit compound naringenin can block the secretion of hepatitis C virus from infected cells, a key step in maintaining chronic infection. This finding suggests that combining naringenin with antiviral medication may allow patients to clear the virus from their livers.
A study published in Clinical Cancer Research found that patients with poor disease-free survival had lower levels of specific microRNAs compared to those with better survival rates. The researchers hope that restoring these microRNAs could lead to improved treatment options for liver cancer patients.
Researchers discovered that midkine can protect liver cells from damage caused by cadmium exposure, promoting hepatocyte proliferation and preventing apoptosis. This finding suggests a potential therapeutic application for midkine in treating cadmium-induced hepatotoxicity.
Researchers at the Salk Institute have created a new chimeric mouse model that can test how drugs affect the liver. The model involves transplanting human hepatocytes into immunodeficient mice, allowing for a natural environment to study drug metabolism and toxicity.
Researchers at MIT have created a novel way to model the full-sized human liver using tiny colonies of living human liver cells. These model livers can survive for up to six weeks and allow for more accurate prediction of drug toxicity, reducing the costs associated with their development.
Researchers at Ohio State University are developing a new technology to keep artificial liver cells alive and functioning normally. By creating different types of hemoglobin-based oxygen carriers, they can recreate natural oxygen gradients, allowing the liver cells to function as well as they do in the body.
Researchers at OHSU have created a technique to produce human liver cells in mice, which can be used to test how pharmaceuticals are metabolized. This innovation has the potential to change the way drugs are tested and could lead to breakthroughs in treating diseases such as hepatitis C and malaria.
Scientists at the University of Texas Medical Branch have discovered a cellular protein, PAK1, that interferes with hepatitis C virus replication. The finding may lead to new drug development to fight the virus, which affects approximately 170 million people worldwide.
Researchers have discovered that liver regeneration is driven by an increase in cell multiplication through regular cell divisions, rather than relying on embryonic-like processes. This finding could lead to more effective ways to stimulate liver growth and potentially improve treatment options for patients with liver diseases.
Researchers found that hypoglycemic neuronal death is triggered by glucose reperfusion and activation of NADPH oxidase. Treatment with CD40Ig allows rats to accept heart grafts from non-genetically identical donors by enhancing regulatory immune cells.
A new device created by MIT researchers allows biologists to physically arrange cells to be touching, close but not touching, or completely separated. This enables researchers to study cell interactions and changes over time without breaching the divide, leading to insights into liver cell differentiation and cancer.
Researchers at UCSD School of Medicine discovered a cellular receptor involved in triggering cell death is also necessary for tissue repair and regeneration after liver injury. p75 neurotrophin receptor promotes the initial activation of hepatic stellate cells to stimulate new hepatic cell proliferation.
Researchers developed a novel virus culture system that enables sustained replication and production of HCV particles in nontransformed hepatocytes. This breakthrough allows for better understanding of HCV differences between strains and may improve treatment strategies.
Researchers discovered that liver cells can activate T cells independently of the lymph system, potentially contributing to impaired immune responses in chronic hepatitis C. The study found that T cells interact with liver cells through fenestrations in sinusoidal endothelial cells.
Researchers at St. Jude Children's Research Hospital have discovered that the protein ABCB6 is crucial for producing heme, a molecule essential for red blood cells to carry oxygen. The team found that ABCB6 helps regulate the production of heme by ferrying in porphyrins, which are then converted into heme inside the mitochondria.
Scientists develop method to introduce purine nucleoside phosphorylase (PNP) enzyme into cells of mice with genetic defect, potentially leading to treatment for individuals lacking PNP. Research also sheds light on scavenger receptor BI's role in protecting against heart disease.
Researchers found that TRAIL can enhance hepatocyte cell death initiated by signaling through Fas, potentially leading to liver damage. The study has important clinical implications as liver cells expressing Fas are present during inflammation.
Researchers used real-time imaging to track malaria infections in live mice, discovering that the parasite uses dead liver cells to cloak and transport itself back into the bloodstream. The study provides insights into the parasite's complex life cycle and potential ways to treat malaria.
A study by UCSD researchers found that the absence of IKKƒÒ in hepatocytes leads to increased JNK activation after exposure to toxic chemicals, resulting in accelerated tumor development. Deletion of JNK1 gene prevented liver cancer, suggesting a critical role for this isoform in tumor growth.
The Smart Petri Dish uses porous silicon crystals filled with polystyrene to detect subtle changes in cell sizes and shapes, allowing for early detection of liver toxicity. The device can perform multiple assays simultaneously and is non-invasive, making it a potential tool for predicting human liver responses.
Researchers at Johns Hopkins Medicine have discovered a protein called GCN5 that plays a crucial role in controlling blood sugar levels. By altering the activity of another protein, PGC-1alpha, GCN5 can turn off pathways leading to glucose release from liver cells.
Research by Chuan-Qing Wang and colleagues found that morphine withdrawal and precipitated withdrawal increase HCV replicon expression and inhibit IFN-alpha production in liver cells. This study suggests that opioid abuse may contribute to the chronicity of HCV infection and promote disease progression.
A new laboratory test has been developed to identify patients at high risk of developing cirrhosis after a liver transplant due to hepatitis C. The test targets hepatic stellate cells, which can produce collagen leading to scarring in infected patients.
Researchers found that reducing clk-1/mclk1 activity promotes longevity in mice, similar to the effect seen in C. elegans. The study also discovered that mclk null cells have a growth advantage due to resistance to oxidative stress.
Researchers identified alpha-smooth muscle actin (alpha-SMA) as a reliable marker for predicting fibrosis development after liver transplant. Studies showed that HSC activation was associated with advanced fibrosis, suggesting a potential biomarker for early intervention and treatment.
A new protein called ABIN-1 has been discovered that can prevent the death of liver cells in people with hepatitis. Researchers have shown that an extra dose of ABIN-1 provides a double protective effect against inflammation and cell death, offering new hope for treating liver disorders.
Researchers at the University of Iowa developed a new gene therapy vector that can effectively deliver therapeutic genes to liver cells, converting Hemophilia A from a severe to a mild form in mice. The correction lasted 30 weeks and showed promise for reducing bleeding episodes in people with hemophilia.
Researchers at UNC School of Medicine used embryonic stem cells treated with a growth factor to reverse hemophilia B in genetically altered mice. The study demonstrates the potential for stem cell therapy in treating genetic disorders, such as liver diseases.
Researchers at Joslin Diabetes Center have identified the critical role of two insulin signaling proteins in controlling glucose and lipid metabolism. By knocking out these proteins in liver cells, they found that diabetes results when both signals are simultaneously low, but not when either is individually depleted.
Researchers at the University of California, San Diego, have developed a technique to identify the precise mix of extracellular matrix proteins that optimally prompts mouse embryonic stem cells to begin differentiating into liver cells. This breakthrough enables scientists to use inexpensive and widely available reagents and machinery ...
Researchers discover how the hepatitis virus's X protein influences liver cell behavior, potentially leading to alternative cancer therapies. The protein's presence in patients' livers could be harnessed to target only cancerous cells.
A single protein, ChREBP, activates genes in liver cells to convert sugar into fat, a process crucial for energy storage. Researchers found that ChREBP directly binds to DNA of fat-formation genes, increasing expression of enzymes.
Researchers found that turning off a single cancer-causing gene can eliminate aggressive liver tumors in mice within four weeks. The discovery involves manipulating the Myc protein, which drives cancer cell division, and has potential applications for treating common types of cancer.