RGS G-protein master regulator --- An Understudied Cause of Cancer: Mutations in Regulators of Cell Signaling

Cancer cell use of glycolysis is mediated by the CtBP family of NADH dependent transcriptional regulators

Tau Protein travels along neurons like vehicles travel on the interstate

Nilotinib appears to aid in the clearance of accumulated beta-amyloid (Abeta) plaques and Tau tangles in neurons in the brain—hallmarks of Alzheimer's disease. Nilotinib appears to penetrate the blood-brain barrier and turn on the "garbage disposal" machinery inside neurons (a process known as autophagy) to get rid of the Tau, Abeta and other toxic proteins.

There are types of bacteria living inside cancer cells and immune cells within tumors

Actin-6 plays a key role in neuronal branching

Fragile X Syndrome, most common genetic cause of autism, is related to FMRP levels (a protein that aids in forming synaptic connections between neurons)

High Levels of Creld2 Protein in Aggressive Types of Breast Cancer. Research suggests that the silicone from breast implants can enter the bloodstream/lymphatic system and cause cell death.

"Our fundamental finding was that these metabolites inhibit an enzyme called KDM4B that regulates the presence of methyl groups on the histones," said Glazer. "The consequence is that there are way too many methyl groups on the histones. That floods the system, so that the damage is masked."

About half of ALS patients also develop dementia. Genetic studies of families with a predisposition to develop ALS have shown that the condition can be associated with certain gene mutations. Some of these mutations involve the gene UBQLN2 which regulates the disposal of misfolded "garbage" from the body's cells. Until now, researchers did not fully understand how UBQLN2 mutations interfere with this pathway and cause ALS.

Exosomes, microscopic packets containing genetic material, are shed by tissues into the blood. By sequencing microRNA within exosomes originating in the brain, it is now possible to definitively distinguish blood samples of ALS patients from healthy controls, a team of researchers at the Brain Chemistry Labs announced today in Open Biology. ALS is a progressive neurodegenerative disease that typically affects people in the prime of their life.

"Recent studies have linked certain forms of kidney disease to proteins called connexins, which normally help to facilitate communication between kidney cells. If these connexins fail, signaling molecules spill into the organ and set off a chain of events that can ultimately lead to kidney failure. One connexin—called Cx43—actually makes the whole situation worse, so our new research set out to effectively block Cx43," said Dr. Hill. "By providing insight into the initiating trigger for early injury in chronic kidney disease, we expose the tantalizing prospect that by altering the tone of conversation between cells we could prevent kidney damage and slow disease progression."

Each day, in human cells, tens of thousands of DNA damage events occur. In cancer cells, the expression of the protein APOBEC3A is one of the most common sources of DNA damage and mutations. While the mutations caused by these particular proteins in cancer cells contribute to tumor evolution, they also cause breaks in the DNA, which offer a vulnerability.

A key feature of neutrophils is their ability to extrude a structure called a neutrophil extracellular trap (NET) into their surroundings. This consists of a web of DNA coated in enzymes toxic to microorganisms, and it can trap and kill invading microbes. But in the lungs, NETs are induced by inflammation, and their tumour-boosting activity has been linked to NET-associated enzymes. A growing body of evidence indicates that NETs mediate the development and enhancement of the invasive properties of cancer cells

Step 2. Write Objectives. Capture with metrics how Android/Iphone applications effectively be integrated in to medical education. Do Android/Iphone applications when effectively integrated into medical education improve student retention and improve clinical skills over time.

Step 1. Create a monkey survey for preliminary research. Question 1. What are the ways in which medical education [pre-clinical years and clinical years] is broken? 2. What are ways that medical education can be reformed? 3. Do you think

Pathological protein clumps are characteristic of a series of diseases, such as Alzheimer's disease, Parkinson's disease, and type 2 diabetes. Scientists at Forschungszentrum Jülich, Heinrich Heine University Düsseldorf, and Maastricht University have now used cryo-electron microscopy to obtain a sharp image for the first time of how individual molecules are arranged in protein strings, which constitute the deposits typical for diabetes. The structure of the fibrils is very similar to that of Alzheimer's fibrils. These findings are in line with other commonalities that researchers have discovered in the last few years. The deposits, known as islet amyloid, comprise tiny protein threads known as fibrils. In the case of diabetes, they consist of the peptide hormone IAPP. In the pancreas, they contribute to the death and dysfunction of beta cells that are responsible for producing insulin.

Student Responses. Students reiterated that there is no need to put so much pressure on exams like the Step exams to determine what you will specialize in.

Remember the gut is connected with the mouth. Oral bacterium should be researched more as diagnostic capability for inflammatory bowel syndrome. A collaborative study by research groups from the VIB-UGent Center for Inflammation Research and Ghent University uncovered a new mechanism causing colorectal cancer. The researchers found that abnormal expression of the protein Zeb2 affects the integrity of the intestinal wall or 'epithelium.' This epithelium normally functions as a barrier to prevent infiltration by intestinal microbes. Zeb2 undermines this barrier and allows infiltrating bacteria to cause inflammation that drives cancer progression. Importantly, the scientists demonstrated that manipulating the immune system or removing the microbiota can prevent the development of cancer. These findings may lead to new treatments and are published in the leading journal Nature Cancer.

FSU Assistant Professor of Psychology Aaron Wilber and graduate student Sarah Danielle Benthem showed that the way two parts of the brain interact during sleep may explain symptoms experienced by Alzheimer's patients, a finding that opens up new doors in dementia research. It is believed that these interactions during sleep allow memories to form and thus failure of this normal system in a brain of a person with Alzheimer's disease may explain why memory is impaired. Wilber and Benthem's study, based on measuring brain waves in mouse models of the disease, gave researchers a number of new insights into Alzheimer's including how the way that two parts of the brain—the parietal cortex and the hippocampus—interact during sleep may contribute to symptoms experienced by Alzheimer's patients, such as impaired memory and cognition, and getting lost in new surroundings.

Statins, a group of drugs commonly prescribed for those with high cholesterol, were shown to interfere with a pathway that allows a cancer cell to recycle cell surface proteins and therefore make it easier for cancer cells to live within the brain.Statins suppress breast cancer survival in the brain by inhibiting the ability of Rab11b to recycle surface proteins

Cancer induced by viruses. causes inflammation and oncogenesis. The action of the viral gene HTLV-1 bZIP factor (HBZ) changes the reactivity of immune cells (T cells) infected with HTLV-1 to cytokines, which results in inflammation. This research is expected to contribute to the understanding of the mechanisms of HTLV-1-induced malignant tumors (ATL) and HTLV-1-related inflammatory diseases, and lead to the development of new treatment and prevention strategies. )

Cancer metastasis moderated by the bioeletrical environment of the tumor

The role of immune cells in cancer metastasis underestimated. NET's traps comprised of a mix of DNA and other compounds by neutrophils is another former finding.

"Over the last couple years, a sea change in dementia and Alzheimer's disease research has occurred. Focus has shifted from solely targeting amyloid-beta in the brain to the opinion that more fruitful progress could be made by addressing factors that compromise the blood brain barrier," explains co-author Mark Carnegie, of The Brain Protection Company based in Australia. "Elements of the constellation include chronic age-related inflammation, genetic predisposition, and cardiovascular abnormalities, notably high blood pulse pressure."Dr. Rachel Levin, lead author of the paper, says that "combination therapy has been paramount in the treatment of other challenging diseases, in particular cancer. Therefore, in dementia, reducing elevated pulse pressure could prove to be synergistic with other therapeutic approaches such as anti-amyloid-beta drugs or stem cell therapy."

SHMT2 is implicated in the spread of lymphoma and demonstrates that not only mutated cells cause cancer but too much of a good protein (methylation of the suppressor region)

Dr. Kermorgant said: "We are very excited with this discovery which suggests that MET, a major cancer target, may be co-targeted with existing drugs against two other major targets, PI3K and mTOR. This could be tested in clinical trials in a near future."

And they conclude: "The identification of increased dementia risk and earlier onset among patients with IBD suggest that [they] might benefit from education and increased clinical vigilance," to slow cognitive decline and improve quality of life.

Apolipoprotein E (ApoE) is kind of like a delivery service for the human brain. It supplies neurons with important nutrients, including with polyunsaturated fatty acids—which are building blocks of the membranes surrounding the neurons. In addition, certain unsaturated fatty acids are converted into so-called endocannabinoids. These are endogenous signaling molecules that regulate many functions of the nervous system such as memory, but also the control of immune response, thereby protecting the brain from inflammation.

Scientists at Uppsala University have discovered a hitherto unknown function of blood platelets in cancer. In mouse models, these platelets have proved to help preserve the vascular barrier which makes blood-vessel walls selectively impermeable, thereby reducing the spread of tumor cells to other parts of the body. The study is published in the journal Cancer Research.

Tau can undergo a variety of modifications during the course of the disease including phosphorylations. Researchers found that the presence of different forms of phosphorylated tau could explain why the disease has variable effects. The researchers found "striking" variation in the presence of phosphorylated tau oligomers that associates with greater tau spread, and, importantly, worse disease. Different specific modifications were associated with different degrees of severity and progression rate.