Not exact matches
Frey's team did not train their system to predict
diseases, but instead to take measurements of contents
within a
cell (metrics such as the concentration of a specific protein) and draw conclusions about the cellular system as a whole.
«By studying the ways different proteins like keratin dynamically change
within a
cell, we can better understand the progression of cancers and other
diseases,» they say.
McCallion's strategy to make sense of all this data looks at the active genes in
cells affected by a
disease, groups of genes that interact with one another, their vulnerability to mutation and information from past scientific studies to filter more than a thousand gene candidates for
disease risk down to just a handful
within any one implicated region.
TANGLED proteins that strangle brain
cells from
within seem to be what allows Alzheimer's
disease to spread through the brain.
Using animal models of precancerous polyps in the bowel, Chung and his team determined that certain types of immune
cells within a chronically inflamed intestine can become rewired, causing them — paradoxically — to contribute to
disease development rather than protect against it.
Since many human
diseases can be explained by perturbations of molecular interactions
within cells, interactomes will drastically change how we think about human health, and how we set about designing drugs and preventive measures to counter illness.
Interdisciplinary research at the University of Pennsylvania is showing how
cells interact over long distances
within fibrous tissue, like that associated with many
diseases of the liver, lungs and other organs.
Moreover, her studies are the first to indicate that therapies targeted at controlling the properties of smooth muscle
cells within lesions may be highly effective in treating a
disease that is the leading cause of death worldwide.
They found that most cases of liver
disease in people with type 2 diabetes are not alcohol - related but caused by a build - up of fat
within liver
cells — a condition known as non-alcoholic fatty liver
disease (NAFLD).
They do their dirty work by infiltrating bacteria, including
disease - causing germs, and destroying them from
within: After latching onto bacteria, the phages bore inside and hijack the bacteria's genetic machinery, turning them into phage factories that eventually make so many copies that the
cells burst, killing off the host.
Subsequent transplant of millions of human T - ALL
cells into normal mice that were then treated with an anti-CXCR4 drug induced remission
within two weeks, with
diseased spleen and bone marrow tissue nearly returning to normal.
In experiments in mice and human
cells, researchers found that blocking CXCR4 — a so - called homing receptor protein molecule that helps T
cells mature and attracts blood
cells to the bone marrow — halted
disease progression in bone marrow and spleen tissue
within two weeks.
Recent advances in our understanding of cancer have revealed that the
disease can not be understood through simple analysis of genetic mutations
within the cancerous
cells.
Recent advances in our understanding of cancer have revealed that the
disease can not be understood through simple analysis of genetic mutations
within cancerous
cells.
Small molecule drugs can be screened or designed to increase telomerase activity exclusively
within stem
cells for
disease treatment as well as anti-aging therapies without increasing the risk of cancer.
«We measured the electrical activity of groups of nerve
cells within the subthalamic nucleus in patients with Parkinson's
disease, who had recently been treated with deep brain stimulation.
By receiving transplants of bone marrow
cells along with the new kidney, four of five transplant patients with end - stage renal
disease were able to stop taking immunosuppressive drugs
within about one year after surgery.
The hope is the technique could be used to unpick the role of proteins in many complex processes, such as the consolidation of memories, or be used to block the interactions between proteins
within cells to help illuminate the processes that underpin
disease.
For example, the camera could be used to visualize energy metabolism as it occurs
within a
cell's mitochondria or the way light passes through tissue, an important consideration for therapies that use lasers to destroy
diseased tissue with the goal of leaving healthy tissue unharmed.
Parkinson's
disease is a slowly progressive
disease that affects a small area of
cells within the mid-brain known as the substantia nigra.
The ability to manipulate specific genes
within these hippocampal chandelier
cells may allow for more meticulous studies of several
diseases, including epilepsy and schizophrenia, in which these neurons have been implicated.
Jiang estimates that human clinical trials could begin
within a decade: «At first, the
cells could be used to treat
diseases with single missing or malfunctioning
cell types, like hemophilia, diabetes, Parkinson's
disease, and muscular dystrophy.
The polymer patch could one day lay down a pathway in areas damaged by heart
disease for
cells to regenerate and regrow, while the mesh itself slowly disintegrates
within the body.
To find out the specific metabolic pathways affected by
disease or stress, the Tufts scientists looked at three parameters: the ratio of FAD to NADH, the fluorescence «fade» of NADH, and the organization of the mitochondria as revealed by the spatial distribution of NADH
within a
cell (the energy producing «batteries» of the
cell).
«Our results suggest that heart failure would be better addressed by treatments that shut down immune
cells that are both sources and targets of cytokines in the spleen and heart, instead of targeting any one cytokine,» said Sumanth Prabhu, M.D., director of the Division of Cardiovascular
Disease within the UAB School of Medicine and study leader.
Within a few weeks, the new
cells were producing mature blood
cells, and the symptoms of sickle
cell disease had dramatically improved, the team reports.
The researchers note that CD8 + T
cells could potentially be used as markers for the progression of fatty liver
disease, which is expected to become the leading indication for liver transplantation
within the next one or two decades.
Molecular microbiologists at the University of Southern California (USC) have uncovered intricate regulatory mechanisms
within the
cell that could lead to novel therapeutics for the treatment of cancer and other
diseases.
The ultimate goal is to produce pluripotent
cells by purely chemical means
within the body to regenerate damaged parts and to treat
disease.
«We have shown for the first time that increasing synaptic connectivity
within engram
cell circuits can be used to treat memory loss in mouse models of early Alzheimer's
disease,» says lead author Dheeraj Roy.
We recently discovered that there are certain ways of limiting protein synthesis
within cells, which is something that happens as a result of dietary restriction, to increase health and resistance to age - related
disease.
DNA damaging agents can promote ageing,
disease and cancer and are widespread in the environment as well as being produced
within human
cells as normal cellular metabolites
We use physiology, histology, and molecular biology to understand development and
disease on a holistic basis, all the way from the individual to the organ to the tissue and finally to the molecules
within cells.
Inclusion Criteria: • Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1 • Have histologically or cytologically confirmed advanced or metastatic non-small
cell lung cancer (NSCLC)(Stage IIIb or greater) • Measurable
disease, as defined by Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 • Known PD - L1 tumor status as determined by an immunohistochemistry (IHC) assay performed by the central laboratory on tissue obtained at Screening • A woman of childbearing potential must have a negative highly sensitive serum (beta - human chorionic gonadotropin [beta - hCG]-RRB- at Screening
within 14 days prior to study drug administration Inclusion Criteria for Crossover: • Participants must have been randomized to Arm A of the study and had radiographic
disease progression according to RECIST 1.1 • Participants must have a mandatory biopsy at the time of
disease progression according to RECIST 1.1 prior to crossing over.
Hidden
within human
cells are the root causes of many
diseases.
Scientists currently know very little about why these particular
cells within the eye do not survive with age and cause problems that lead to a
disease called Pigment Dispersion Syndrome (PDS).
The genes identified by this study may implicate pathways involved in inflammation, movement of proteins
within cells, and lipid transport as being important in the
disease process.
«We have shown for the first time that increasing synaptic connectivity
within engram
cell circuits can be used to treat memory loss in mouse models of early Alzheimer's
disease,» said lead author Dheeraj Roy in a release.
The massive number of
cells within the OSVZ of humans «tells us we have to be careful when modeling human brain
diseases in mice,» says Kriegstein.
The ability of the tumor
cells to metastasize locally
within the brain is a significant clinical problem, which causes the
disease to recur even after the original tumor is surgically removed.
The disorganization of the genetic material (DNA)
within cells can have dire consequences for the health of an organism, ultimately resulting in death or
disease.
• Patients must have adequate coagulation (international normalized ratio (INR) or prothrombin time (PT), partial thromboplastin time (PTT) ≤ 1.5 times ULN) • Adequate liver function (total bilirubin ≤ 1.5 times the ULN, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) ≤ 2.5 times ULN Exclusion Criteria: • Presence of active / uncontrolled central nervous system involvement • History of clinically significant cardiac
disease; uncontrolled hypertension • Left ventricular ejection fraction (LVEF) < 45 % • Allogeneic stem
cell transplant
within 100 days before first dose of study drug • Known history of human immunodeficiency virus (HIV) infection • Chronic or active hepatitis B or C, requiring antiviral therapy • Evidence of history of bleeding disorder, dialysis, or coexisting cancer that is distinct in primary site or histology from the cancer evaluated in this study • Serious, uncontrolled infection • Unresolved chronic toxicity > grade 1 from prior therapy • Use of strong CYP3A4 inhibitors or strong inducers
within 7 days prior to the start of study treatment and for the duration of the study
The Tissue Platform workgroup
within autoimmune inflammatory
diseases at Karolinska Institutet studies the effects of probes in
cell assays relevant for the
diseases we study, ie systemic lupus erythematosus, idiopathic inflammatory myositis, systemic sclerosis and inflammatory bowel
disease.
We investigate how changes to DNA organization
within the nucleus of a
cell impact development and
disease.
Many
diseases kill
cells within organs, claiming lives or impairing a person's ability to live a normal life.
«If we could really describe how
diseases change molecules in specific
cells within the living brain, it might enable better drug targets to be found.»
Her current research is focused on discovering how normal and
disease melanocyte
cell states establish distinct regulatory DNA landscapes, and also determining how the combination of both genetic variation
within these regulatory regions and environmental
cell signals alter gene expression and normal
cell function.
On the surface, the
disease appears relatively simple, with high pressure (intra-ocular pressure, or IOP)
within the eye associated with the death of
cells in the retina and optic nerve dysfunction.
Kmiec noted that while some ailments, like sickle
cell anemia and Huntington's
disease, involve faulty DNA
within a single gene, others, like Alzheimer's and heart
disease, appear to involve malfunctions in multiple genes where the best option «is not really gene editing, but gene replacement.»
The antiviral restriction factor IFN - induced transmembrane protein 3 (IFITM3) inhibits
cell entry of a number of viruses, and genetic diversity
within IFITM3 determines susceptibility to viral
disease in humans.