[The Washington Post] Scientists have created a new blood test that can detect every virus that has ever infected an individual.
Pasquale Valente's insight:
"The new test, known as VirScan, works by screening the blood for antibodies against any of the 206 species of viruses known to infect humans, according to a study published Thursday in the journal Science. "
The consumer technology companies that own desktop software, Web search, and mobile phones have set themselves a new goal. They’re aiming to carve themselves a slice of health care, the US $3 trillion industry that represents nearly a fifth of the U.S. economy.
There’s a lot at stake here, and not just financially. Pundits have described a future in which your body is minutely and continuously monitored. Your wearables and assorted wireless-enabled gadgets—your bathroom scale, perhaps a blood-glucose monitor—would gather torrents of physiological data. Someday, the data might even come from biosensors worn on the body, like tattoos, or ultimately, from implanted devices. This flood of info would sluice to your smartphone before streaming off to the cloud. Apps could continuously monitor the data and, if it took an alarming turn, bring it to the attention of a medical professional. Although the quantities of data might well be huge, this vision could be realized with technologies available now or anticipated soon.
LAWRENCEVILLE, N.J., May 21, 2015 /PRNewswire/ -- Celsion Corporation (NASDAQ: CLSN), a fully-integrated oncology company focused on the development of a portfolio of innovative cancer treatments, including directed chemotherapies, immunotherapies and RNA- or DNA-based therapies for the treatment of cancer and other difficult-to-treat diseases, today reported data from a preclinical study confirming that the Company's TheraSilence™ technology platform can safely and effectively deliver RNA to the lungs in non-human primates. TheraSilence™ is designed to enable the delivery of synthetically-generated mRNA, inhibitory RNA (RNAi) such as small inhibitory RNAs (siRNAs), microRNAs, microRNA mimics, and related molecules that can regulate protein expression at the transcript level by exploiting endogenous cell mechanisms.
Inhibitors of PARP-1(Poly(ADP-ribose) polymerase-1) act by competing with NAD+, the enzyme physiological substrate, which play a protective role in many pathological conditions characterized by PARP-1 overactivation. It has been shown that PARP-1 also promotes tumor growth and progression through its DNA repair activity. Since angiogenesis is an essential requirement for these activities, we sought to determine whether PARP inhibition might affect rat brain microvascular endothelial cells (GP8.3) migration, stimulated by C6-glioma conditioned medium (CM). Through wound-healing experiments and MTT analysis, we demonstrated that PARP-1 inhibitor PJ-34 [N-(6-Oxo-5,6-dihydrophenanthridin-2-yl)-N,N-dimethylacetamide] abolishes the migratory response of GP8.3 cells and reduces their viability. PARP-1 also acts in a DNA independent way within the Extracellular-Regulated-Kinase (ERK) signaling cascade, which regulates cell proliferation and differentiation. By western analysis and confocal laser scanning microscopy (LSM), we analyzed the effects of PJ-34 on PARP-1 expression, phospho-ERK and phospho-Elk-1 activation. The effect of MEK (mitogen-activated-protein-kinase-kinase) inhibitor PD98059 (2-(2-Amino-3-methoxyphenyl)-4 H-1-benzopyran-4-one) on PARP-1 expression in unstimulated and in CM-stimulated GP8.3 cells was analyzed by RT-PCR. PARP-1 expression and phospho-ERK activation were significantly reduced by treatment of GP8.3 cells with PJ-34 or PD98059. By LSM, we further demonstrated that PARP-1 and phospho-ERK are coexpressed and share the same subcellular localization in GP8.3 cells, in the cytoplasm as well as in nucleoplasm. Based on these data, we propose that PARP-1 and phospho-ERK interact in the cytosol and then translocate to the nucleus, where they trigger a proliferative response. We also propose that PARP-1 inhibition blocks CM-induced endothelial migration by interfering with ERK signal-transduction pathway.
Despite advances in analyzing tumor biology, choosing effective therapies for cancer patients remains difficult. This is partly because there are still no timely, foolproof ways to test whether a patient will respond to a particular treatment. Addressing this issue, two independent teams—one at the Fred Hutchinson Cancer Research Center in Seattle and another at MIT—have developed devices that can test a tumor’s response to multiple cancer drugs directly in the patient. Both devices are described today (April 22) in Science Translational Medicine.
If validated in human clinical studies, the devices—which are being further developed by spinoff companies—could be used before surgery to help identify the best course of individualized treatment for certain cancer patients.
Researchers at the University of Cambridge have grown functional "mini-lungs" using stems cells derived from the skin cells of patients with a debilitating lung disease. Not only can the development help them in coming up with effective treatments for specific lung diseases like cystic fibrosis, but the process has the potential to be scaled up to screen thousands of new compounds to identify potential new drugs.
Creating miniature organoids has been the focus of many a research group, as it allows scientists to better understand the processes that take place inside an organ, figure out how specific diseases occur and develop or even work towards creating bioengineered lungs.
The research team from the Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute studied a lung disease called cystic fibrosis, which is caused by genetic mutation and shortens a patient's average lifespan. Patients have great difficulty breathing as the lungs are overwhelmed by thickened mucus.
To create working mini-lungs, the researchers took skin cells from patients with the most common form of cystic fibrosis and reprogrammed them to an induced pluripotent state (iPS), which allows the cells to grow into a different type of cell inside the body.
by Young-Ho Lee, Xiyong Liu, Fuming Qiu, Timothy R. O’Connor, Yun Yen, David K.
Members of the heterochromatin protein 1 family (HP1α, β and γ) are mostly associated with heterochromatin and play important roles in gene regulation and DNA damage response. Altered expression of individual HP1 subtype has profound impacts on cell proliferation and tumorigenesis. We analyzed the expression profile of HP1 family by data mining using a published microarray data set coupled with retrospective immunohistochemistry analyses of archived breast cancer biospecimens. We found that the patient group overexpressing HP1βmRNA is associated with poorly differentiated breast tumors and with a significantly lower survival rate. Immunohistochemical staining against HP1α, HP1β and HP1γ shows that respective HP1 expression level is frequently altered in breast cancers. 57.4 - 60.1% of samples examined showed high HP1β expression and 39.9 - 42.6 % of examined tumors showed no or low expression of each HP1 subtype. Interestingly, comparative analysis on HP1 expression profile and breast cancer markers revealed a positive correlation between the respective expression level of all three HP1 subtypes and Ki-67, a cell proliferation and well-known breast cancer marker. To explore the effect of individual HP1 on PARP inhibitor therapy for breast cancer, MCF7 breast cancer cells and individually HP1-depleted MCF7 cells were treated with PARP inhibitor ABT-888 with or without carboplatin. Notably, HP1β-knockdown cells are hypersensitive to the PARP inhibitor ABT-888 alone and its combination with carboplatin. In summary, while increased HP1β expression is associated with the poor prognosis in breast cancer, compromised HP1β abundance may serve as a useful predictive marker for chemotherapy, including PARP inhibitors against breast cancer.
The immune system can remember a previously experienced pathogen and can evoke an enhanced response to reinfection that depends on memory lymphocyte populations. Recent advances in tracking antigen-experienced memory B cells have revealed the existence of distinct classes of cells that have considerable functional differences. Some of these differences seem to be determined by the stimulation history during memory cell formation. To induce rapid recall antibody responses, the contributions of other types of cells, such as memory T follicular helper cells, have also now begun to be appreciated. In this Review, we discuss these and other recent advances in our understanding of memory B cells, focusing on the underlying mechanisms that are required for rapid and effective recall antibody responses.
An international, randomized, phase III study has analyzed the DNA of 503 patients with metastatic colorectal cancer by liquid biopsy (BEAMing platform) to detect KRAS, PIK3CA and BRAF gene mutations in tumors.
Neuroscientists have uncovered a previously unknown direct connection between the brain and the immune system -- a finding that could have significant implications for the treatment of brain disorders
Pasquale Valente's insight:
"While previous research held that there was no direct connection between the brain and the lymphatic system, the new findings, which were recently published in the journal Nature, present a model of the lymphatic system that includes the brain."
Plants respond to pathogens using elaborate networks of genetic interactions. Recently, significant progress has been made in understanding RNA silencing and how viruses counter this apparently ubiquitous antiviral defense. In addition, plants also induce hypersensitive and systemic acquired resistance responses, which together limit the virus to infected cells and impart resistance to the noninfected tissues. Molecular processes such as the ubiquitin proteasome system and DNA methylation are also critical to antiviral defenses. Here, we provide a summary and update of advances in plant antiviral immune responses, beyond RNA silencing mechanisms—advances that went relatively unnoticed in the realm of RNA silencing and nonviral immune responses. We also document the rise of Brachypodium and Setaria species as model grasses to study antiviral responses in Poaceae, aspects that have been relatively understudied, despite grasses being the primary source of our calories, as well as animal feed, forage, recreation, and biofuel needs in the 21st century. Finally, we outline critical gaps, future prospects, and considerations central to studying plant antiviral immunity. To promote an integrated model of plant immunity, we discuss analogous viral and nonviral immune concepts and propose working definitions of viral effectors, effector-triggered immunity, and viral pathogen-triggered immunity.
Your doctor may order a test for circulating tumor cells (CTCs) to help guide your cancer care. One of the major challenges in treating cancer is getting “all” of the cancer, including the parts we cannot see. Even if surgery, chemotherapy, or radiation removes all traces of known cancer, there...
The ubiquitin system produces a protein that greatly restricts the development of cancerous tumors.
A new study by researchers at the Technion-Israel Institute of Technology could hold one key to control cancer cell growth and development. In a paper published in the April 9, 2015 edition of CELL, the team reports on the discovery of two cancer-suppressing proteins.
Distinguished Professor Aaron Ciechanover. Photographer: Dan Porges
The research was conducted in the laboratory of Distinguished Professor Aaron Ciechanover, of the Technion Rappaport Faculty of Medicine. The team was led by research associate Dr. Yelena Kravtsova-Ivantsiv and , included additional research students and colleagues, as well as physicians from the Rambam, Carmel and Hadassah Medical Centers, who are studying tumors and their treatment.
The heretofore-undiscovered proteins were found during ongoing research on the ubiquitin system, an important and vital pathway in the life of the cell, which is responsible for the degradation of defective proteins that could damage the cell if not removed. The ubiquitin system tags these proteins and sends them for destruction in the cellular complex known as the proteasome. The system also removes functional and healthy proteins that are not needed anymore, thereby regulating the processes that these proteins control.
Usually, the proteins that reach the proteasome are completely broken down, but there are some exceptions, and the current line of research examined p105, a long precursor of a key regulator in the cell called NF-κB. It turns out that p105 can be broken down completely in certain cases following its tagging by ubiquitin, but in other cases it is only cut and shortened and becomes a protein called p50.
NF-κB has been identified as a link between inflammation and cancer. The hypothesis of the connection between inflammatory processes and cancer was first suggested in 1863 by German pathologist Rudolph Virchow, and has been confirmed over the years in a long series of studies. Ever since the discovery (nearly 30 years ago) of NF-κB, numerous articles have been published linking it to malignant transformation. It is involved in tumors of various organs (prostate, breast, lung, head and neck, large intestine, brain, etc.) in several parallel ways, including: inhibition of apoptosis (programmed cell death) normally eliminates transformed cells; acceleration of uncontrolled division of cancer cells; formation of new blood vessels (angiogenesis), which are vital to tumor growth; and increased resistance of cancerous cells to irradiation and chemotherapy.
The dramatic effect of these proteins on cancer growth: above the two tumors in the foreground (the control group) are tumors that express high levels of the proteins
As noted, the precursor p105 is “handled” by the ubiquitin system in one of two parallel and equally prevalent ways. It is either destroyed completely, or shortened and transformed to p50. The current research deciphers the decision-making mechanism that determines which process will be applied to the protein: when a ubiquitin system component called KPC1 is involved in the process and attaches ubiquitin to p105, the protein is shortened to become p50. When ubiquitination is mediated by another component of the system (and without KPC1), p105 is degraded.
The ubiquitin molecule within all living cells
The decision between these two options has significant implications on the cell, as the presence of high levels of KPC1 (which generates p50) and p50 (the product of the process) – with the accompanying disruption of the normal ratios between the processes – suppresses the malignant growth and apparently protects the healthy tissue. The current research was conducted on models of human tumors grown in mice, as well as on samples of human tumors, and a strong connection was discovered between the suppression of malignancy and the level of the two proteins, clearly indicating that the increased presence of KPC1 and/or p50 in the tissue can protect it from cancerous tumors.
Professor Ciechanover, who is also the president of the Israel Cancer Society, notes that many more years are required “to establish the research and gain a solid understanding of the mechanisms behind the suppression of the tumors. The development of a drug based on this discovery is a possibility, although not a certainty, and the road to such a drug is long and far from simple.”
Professor Ciechanover won the Nobel Prize in Chemistry in 2004 (jointly with Professors Avram Hershko – also from the Technion – and Irwin Rose, of the Fox Chase Cancer Center) for the discovery of the ubiquitin system. The current line of research is a continuation of that discovery.
For further details: Gil Lainer – 058-6882208, Doron Shaham – 050-3109088.
Scientists working in the area of pancreatic cancer research have uncovered a technique that sees cancerous cells transform back into normal healthy cells. The method relies in the introduction of a protein called E47, which bonds with particular DNA sequences and reverts the cells back to their original state.
The study was a collaboration between researchers at the Sanford-Burnham Medical Research Institute, University of California San Diego and Purdue University. The scientists are hopeful that it could help combat the deadly disease in humans.
"For the first time, we have shown that over-expression of a single gene can reduce the tumor-promoting potential of pancreatic adenocarcinoma cells and reprogram them toward their original cell type," says Pamela Itkin-Ansari, adjunct professor at Sanford-Burnham and lead author of the study. "Thus, pancreatic cancer cells retain a genetic memory which we hope to exploit."
(MedicalXpress)—Resting state networks (RSNs) in the brain are topographies of neural structures between which lag states propagate due to fluctuations of physical and other activities. Studying these networks reveals information about the functional connectivity of neural structures and regions. Results from various studies have confirmed that brain activity is spatially structured, linked to the representation of function, and has clinical relevance.
Functional connectivity is different from the brain's structural connectivity, which describes brain regions that are anatomically attached to each other. Regions with no structural connectivity can nonetheless have functional connectivity as nodes in a functionally connected RSN. Many common RSNs have been mapped in healthy subjects, and researchers believe that understanding the relationships between these networks can contribute to a fundamental model of brain function.
One of the tremendous advantages of functional magnetic resonance imaging (fMRI) is the ability to study brain functional activity without the need for subjects to perform complex tasks. Using fMRI to study resting-state functional connectivity yields a wealth of information about different stages of consciousness and patterns of synchronous activity. One of the neurological features that has emerged from such research is the existence of lags in intrinsic activity as represented by fluctuations of the blood-oxygen level-dependent signals (BOLDs), which are temporally synchronous within the somatomotor system.
Last year, researchers at the departments of radiology and neurology at Washington University published an analysis demonstrating that, contrary to the belief that BOLDs were synchronous with resting state networks (RSNs), the lag topography of BOLDs and RSNs is actually orthogonal. Additionally, they established that BOLDs are not attributable to hemodynamic factors and have neural origin.
By examining more than 3,600 postmortem brains, researchers at Mayo Clinic's campuses in Jacksonville, Florida, and Rochester, Minnesota, have found that the progression of dysfunctional tau protein drives the cognitive decline and memory loss seen in Alzheimer's disease. Amyloid, the other toxic protein ...
Strokes, heart attacks, and traumatic brain injuries are separate diseases with certain shared pathologies that achieve a common end: cell death and human injury due to hypoxia, or lack of oxygen.
In these diseases, a lack of blood supply to affected tissues begins a signaling pathway that ultimately halts the production of energy-releasing ATP molecules — a death sentence for most cells.
By employing derivatives of humanin, a naturally occurring peptide encoded in the genome of cellular mitochondria, researchers at Ben Gurion University of the Negev are working to interrupt this process,
Sharing your scoops to your social media accounts is a must to distribute your curated content. Not only will it drive traffic and leads through your content, but it will help show your expertise with your followers.
How to integrate my topics' content to my website?
Integrating your curated content to your website or blog will allow you to increase your website visitors’ engagement, boost SEO and acquire new visitors. By redirecting your social media traffic to your website, Scoop.it will also help you generate more qualified traffic and leads from your curation work.
Distributing your curated content through a newsletter is a great way to nurture and engage your email subscribers will developing your traffic and visibility.
Creating engaging newsletters with your curated content is really easy.