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MIT’s fast synthesis system could boost peptide-drug development | KurzweilAI

MIT’s fast synthesis system could boost peptide-drug development | KurzweilAI | Salus (Health) | Scoop.it

Small protein fragments, also called peptides, are promising as drugs because they can be designed for very specific functions inside living cells, but manufacturing the peptides takes several weeks, making it difficult to obtain large quantities, and to rapidly test their effectiveness.

 

A team of MIT chemists and chemical engineers has designed a way to manufacture peptides in mere hours. The new system, described in a recent issue of the journal ChemBioChem, could have a major impact on peptide drug development, says Bradley Pentelute, an assistant professor of chemistry and leader of the research team.

 

 


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P4 (predictive, preventive, personalized, partecipatory) medicine
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A Distinct Function of Regulatory T Cells in Tissue Protection: Cell

A Distinct Function of Regulatory T Cells in Tissue Protection: Cell | Salus (Health) | Scoop.it

Highlights

 

•Treg cells serve as a major early source of amphiregulin during influenza infection•Amphiregulin expression in Treg cells is dispensable for their suppressor function•Amphiregulin deficiency in Treg cells results in severe damage of infected lungs•Treg cell production of amphiregulin is IL-18/IL-33 dependent but TCR independent

 

Summary

Regulatory T (Treg) cells suppress immune responses to a broad range of non-microbial and microbial antigens and indirectly limit immune inflammation-inflicted tissue damage by employing multiple mechanisms of suppression. Here, we demonstrate that selective Treg cell deficiency in amphiregulin leads to severe acute lung damage and decreased blood oxygen concentration during influenza virus infection without any measureable alterations in Treg cell suppressor function, antiviral immune responses, or viral load. This tissue repair modality is mobilized in Treg cells in response to inflammatory mediator IL-18 or alarmin IL-33, but not by TCR signaling that is required for suppressor function. These results suggest that, during infectious lung injury, Treg cells have a major direct and non-redundant role in tissue repair and maintenance—distinct from their role in suppression of immune responses and inflammation—and that these two essential Treg cell functions are invoked by separable cues.


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Krishan Maggon 's curator insight, August 31, 7:52 PM

Cell  

Volume 162, Issue 5, p1078–1089, 27 August 2015 A Distinct Function of Regulatory T Cells in Tissue ProtectionNicholas Arpaia, Jesse A. Green, Bruno Moltedo, Aaron Arvey, Saskia Hemmers, Shaopeng Yuan, Piper M. Treuting,Alexander Y. Rudensky DOI: http://dx.doi.org/10.1016/j.cell.2015.08.021
Gilbert Faure au nom de l'ASSIM's curator insight, September 1, 3:20 AM

mucosal immunity, lung, breast ductal epithelia

Gilbert Faure au nom de l'ASSIM's curator insight, September 1, 3:21 AM

AREG

Shoyab M, Plowman GD, McDonald VL, Bradley JG, Todaro GJ (February 1989). "Structure and function of human amphiregulin: a member of the epidermal growth factor family". Science 243 (4894 Pt 1): 1074–6. doi:10.1126/science.2466334. PMID 2466334.

 

 Immunity. 2013 Feb 21;38(2):275-84. doi: 10.1016/j.immuni.2012.09.023. Epub 2013 Jan 17.

Amphiregulin enhances regulatory T cell-suppressive function via the epidermal growth factor receptor.Zaiss DM1, van Loosdregt J, Gorlani A, Bekker CP, Gröne A, Sibilia M, van Bergen en Henegouwen PM, Roovers RC, Coffer PJ, Sijts AJ.Author information1Department of Infectious Diseases & Immunology, Faculty of Veterinary Medicine, University of Utrecht, 3584 CL Utrecht, The Netherlands. d.zaiss@uu.nlAbstract

Epidermal growth factor receptor (EGFR) is known to be critically involved in tissue development and homeostasis as well as in the pathogenesis of cancer. Here we showed that Foxp3(+) regulatory T (Treg) cells express EGFR under inflammatory conditions. Stimulation with the EGF-like growth factor Amphiregulin (AREG) markedly enhanced Treg cell function in vitro, and in a colitis and tumor vaccination model we showed that AREG was critical for efficient Treg cell function in vivo. In addition, mast cell-derived AREG fully restored optimal Treg cell function. These findings reveal EGFR as a component in the regulation of local immune responses and establish a link between mast cells and Treg cells. Targeting of this immune regulatory mechanism may contribute to the therapeutic successes of EGFR-targeting treatments in cancer patients.

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‘Tricorder’-style handheld MouthLab detects patients’ vital signs, rivaling hospital devices | KurzweilAI

‘Tricorder’-style handheld MouthLab detects patients’ vital signs, rivaling hospital devices | KurzweilAI | Salus (Health) | Scoop.it
Inspired by the Star Trek tricorder, engineers and physicians at the Johns Hopkins University School of Medicine have developed a hand-held, battery-powered device called MouthLab that quickly picks up vital signs from a patient’s lips and fingertip.

Updated versions of the prototype could replace the bulky, restrictive monitors now used to display patients’ vital signs in hospitals and actually gather more data than is typically collected during a medical assessment in an ambulance, emergency room, doctor’s office, or patient’s home.

The MouthLab prototype’s measurements of heart rate, blood pressure, temperature, breathing rate, and blood oxygen from 52 volunteers compared well with vital signs measured by standard hospital monitors. The device also takes a basic electrocardiogram. The study was published in the September issue of the Annals of Biomedical Engineering.

Early warning for non-doctors

“We see it as a ‘check-engine’ light for humans,” says the device’s lead engineer, Gene Fridman, Ph.D., an assistant professor of biomedical engineering and of otolaryngology–head and neck surgery at Johns Hopkins. “It can be used by people without special training at home or in the field.” He expects the device may be able to detect early signs of medical emergencies, such as heart attacks, or avoid unnecessary ambulance trips and emergency room visits when a patient’s vital signs are good.

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Controlling inflammation to reduce chronic disease risk | KurzweilAI

Controlling inflammation to reduce chronic disease risk | KurzweilAI | Salus (Health) | Scoop.it
In an open-access paper in the British Journal of Nutrition, a coalition of 17 experts explain how elevated unresolved chronic inflammation is involved a range of chronic diseases, and how nutrition influences inflammatory processes and helps reduce chronic risk of diseases.

According to the authors, “the nutrition status of the individual with for example a deficiency or excess of certain micronutrients (e.g. folate, vitamin B12, vitamin B6, vitamin 1, vitamin E, zinc) may lead to an ineffective or excessive inflammatory response.

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Liquid biopsy identifies mutations in colorectal cancer undetected in tissue ... - Medical Xpress

Liquid biopsy identifies mutations in colorectal cancer undetected in tissue ... - Medical Xpress | Salus (Health) | Scoop.it
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.

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FDA Approves Brain Stimulation Device for Parkinson's Disease

FDA Approves Brain Stimulation Device for Parkinson's Disease | Salus (Health) | Scoop.it
Brio Neurostimulation System is second such device approved for tremor disorders

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Pacific Cove's curator insight, June 16, 3:19 AM

 Once activated, the device sends continuous electrical pulses to the target areas in the brain, blocking the impulses that cause tremors.  #Parkinson's #ALS #Tremors #Caregivers #Caregiving 

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Previously Unknown Link Found Between Brain And Immune System

Previously Unknown Link Found Between Brain And Immune System | Salus (Health) | Scoop.it
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."

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Plant Cell: Plant Immune Responses Against Viruses: How Does a Virus Cause Disease? (2013)

Plant Cell: Plant Immune Responses Against Viruses: How Does a Virus Cause Disease? (2013) | Salus (Health) | Scoop.it

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.


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Andres Zurita's curator insight, May 29, 2013 8:28 AM

Open Access pdf

María Serrano's curator insight, June 24, 2014 12:30 PM
Respuesta inmune de las plantas frente a los virus.
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Circulating Tumor Cells

Circulating Tumor Cells | Salus (Health) | Scoop.it
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...

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Krishan Maggon 's curator insight, May 21, 2:09 PM

Patient Education   JAMA Oncology

 

JAMA Oncology Patient Page | May 21, 2015Circulating Tumor Cells FREE ONLINE FIRSTHoward (Jack) West, MD; Jill O. Jin, MD, MPHJAMA Oncol. Published online May 21, 2015. doi:10.1001/jamaoncol.2015.0711
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Breakthrough in Cancer Research | Technion – Israel Institute of Technology

Breakthrough in Cancer Research | Technion – Israel Institute of Technology | Salus (Health) | Scoop.it
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.

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What If Bacteria Could Be Made to Detect Cancer, Signal its Presence and Treat the Cancer? Well it is Possible!

What If Bacteria Could Be Made to Detect Cancer, Signal its Presence and Treat the Cancer? Well it is Possible! | Salus (Health) | Scoop.it

Synthetic biologist Tal Danino had a thought: What if we could create a probiotic, edible bacteria that was "programmed" to find liver tumors?


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Graham Player Ph.D.'s curator insight, May 11, 4:10 AM

Our body is like a complex eco-system and provides a habitat for bacteria and other organisms. In fact 90% of the cells in our body are bacteria cells, not human cells, each containing their own genetic makeup. They provide essential life-support to our physiological processes, and are collectively known as our microbiome which evolves just as we do.

Today it is possible to modify and program the DNA of bacteria cells, and this experimentation is being done. Bacteria can naturally exist and grow inside of tumors. Especially when you consider that tumors may be areas where the immune system has limited access.

So synthetic biologist, Tal Danino, had a left-field thought: What if we could create a probiotic, edible bacteria that was "programmed" to find liver tumors? He created a programmed-probiotic bacteria that would detect particular bacteria inside a liver tumor, and (via programmed DNA) produce a particular color in the urine as a marker for the presence of the tumor. He then went on to program the probiotic bacteria to not only detect the tumor but also to produce therapeutic molecules from within the tumor environment to shrink the existing tumors. His experiments showed that all of this was possible and successful using a mouse-model.

The ability to program bacteria opens up new possibilities and paths of thinking for dealing with cancer and other diseases.

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Protein converts pancreatic cancer cells back into healthy cells

Protein converts pancreatic cancer cells back into healthy cells | Salus (Health) | Scoop.it
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."

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Toward a model of synchrony in brain networks

Toward a model of synchrony in brain networks | Salus (Health) | Scoop.it
(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.

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Maritha dotws's curator insight, April 4, 8:48 AM

Click here to get more info ... http://sh.st/gYGy5

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Study of thousands of brains reveals tau as driver of Alzheimer's disease

Study of thousands of brains reveals tau as driver of Alzheimer's disease | Salus (Health) | Scoop.it
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 ...

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Cancer Cells Can be Re-Programmed to Become Normal Cells

Cancer Cells Can be Re-Programmed to Become Normal Cells | Salus (Health) | Scoop.it

A team of scientists from Mayo Clinic in Florida have managed to reverse the progress of cancer by “reprogramming” its cells preventing further tumor growth.


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Graham Player Ph.D.'s curator insight, August 26, 2:20 AM

The mechanism behind how cancer cells become malignant has been the focus of many biological studies. Recent research done at the Department of Cancer Biology at Mayo Clinic's Florida campus has revealed a major step forward in further understanding this mechanism.

The process by which normal cells undergo the transition to become tumorigenic has become much clearer. This discovery could change the way we think about cancer progression and open up other avenues of consideration, confirmation and study.

Cells bind together as a normal part of the process of maintaining biological health and the integrity of organs, tissues and structures. The binding together is facilitated by adhesion molecules which are proteins located on the cell surface involved in binding with other cells or with the extracellular matrix. In effect they act like glue to help cells stick to each other and to their surroundings. However it has been known for many years that these adhesion molecules also play another important signaling role.

Both the shape and the physiology of cancer cells are irregular in comparison to normal health cells. In cancer cells the adhesion molecules no longer form particular structures that enable cells to connect, and they signal by turning on or off certain microRNA molecules. These microRNAs are a recently discovered class of non-coding RNAs that play key roles in the regulation of gene expression which can result in alteration of the program of cell growth.

In normal cells the adhesion molecules regulate microRNAs and signal to inhibit cell growth. In cancer cells the absence of the adhesion molecules results in lack of microRNA signaling to inhibit cell growth. This leads to uncontrolled growth of the cancer cells.

The Mayo Clinic study identified the two key components of the adhesion structures and the microRNAs. One drives tumor progression and growth, and the other is acting in opposition by inhibiting that process. In the majority of tumor samples they found that the inhibition component is missing, while the component that drives tumor progression and growth remains active and unopposed.

The study also found that by reintroducing the deregulated microRNAs that inhibit cell growth into cancer cells, it had the effect of reprogramming the cancer cells to become normal cells again. This is a critical turning point in understanding the biology of cancer and how it may be therapeutically addressed.

The challenge that remains is to find the delivery method of introducing the deregulated microRNAs into the cancer cells to regulate the expression of the genes that will reprogram cancer cells to normal cells.

Another benefit of this research is that it may lead to more definitive diagnostic conclusions from biopsies in terms of identifying the presence of cancer. If deregulation of the adhesion signaling is found to be present, then it may determine the presence of cancer.

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European Code Against Cancer, 4th edition: Tobacco and cancer. - PubMed - NCBI

European Code Against Cancer, 4th edition: Tobacco and cancer. - PubMed - NCBI | Salus (Health) | Scoop.it
Cancer Epidemiol. 2015 Aug 10. pii: S1877-7821(15)00129-0. doi: 10.1016/j.canep.2015.06.001. [Epub ahead of print]
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A Conserved Circular Network of Coregulated Lipids Modulates Innate Immune Responses: Cell

A Conserved Circular Network of Coregulated Lipids Modulates Innate Immune Responses: Cell | Salus (Health) | Scoop.it
RT @CellCellPress: A circular network of #sphingolipids and glycerophospholipids regulates innate #immunity: http://t.co/2XspkOcwMO! http:…

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Gilbert Faure au nom de l'ASSIM's curator insight, July 13, 4:26 AM
Highlights

 

•Coregulation between membrane lipid species is organized in a circular network•The lipid network is conserved and reflects metabolism, localization, and adaptation•Sphingolipid metabolism regulates TLR trafficking, signaling, and cytokine release•Network-wide functional lipid annotations predict TLR responses in patient cells

 

An OPEN ACCESS article

Krishan Maggon 's curator insight, July 13, 4:49 AM

Cell  

Volume 162, Issue 1, p170–183, 2 July 2015 A Conserved Circular Network of Coregulated Lipids Modulates Innate Immune ResponsesMarielle S. Köberlin5, Berend Snijder5, Leonhard X. Heinz, Christoph L. Baumann4, Astrid Fauster, Gregory I. Vladimer,Anne-Claude Gavin, Giulio Superti-Furga4Present address: Austrianni GmbH, 1030 Vienna, Austria5Co-first authorOpen AccessDOI: http://dx.doi.org/10.1016/j.cell.2015.05.051 | Article Info
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Cancer Signaling Pathways and Tumor Progression: Images of Biological Processes in the Voice of a Pathologist Cancer Expert

Cancer Signaling Pathways and Tumor Progression: Images of Biological Processes in the Voice of a Pathologist Cancer Expert | Salus (Health) | Scoop.it
Cancer Signaling Pathways and Tumor Progression: Images of Biological Processes in the Voice of a Pathologist Cancer Expert Author and Illustration Curator: Larry H Bernstein, MD, FCAP and Curator:...

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This blood test can tell you every virus you’ve ever had

This blood test can tell you every virus you’ve ever had | Salus (Health) | Scoop.it
[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. "

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The Tech Giants’ Plan to Mine Our Bodies for Data—and Profit

The Tech Giants’ Plan to Mine Our Bodies for Data—and Profit | Salus (Health) | Scoop.it
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.

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Richard Platt's curator insight, May 29, 6:21 PM

The heavyweight corporate muscle behind the vision comes from Apple, Google, Microsoft, and Samsung, which have all launched e-health initiatives, mostly based around smartphones and wearables. Indeed, the fast-growing health care business would seem a natural next step for the tech giants. Technology, including the sort of high-volume digital technology inside smartphones, is playing an increasingly important role in health care. And billions of dollars are now being spent converting the paper-based charts that doctors have long used into modern digital records. Devices, digital data—that’s what these tech giants do. Why shouldn’t they do it in health care, too?

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Celsion Potent, Durable Preclinical Lung Expression Data for Its Novel TheraSilence™ RNA Program

Celsion Potent, Durable Preclinical Lung Expression Data for Its Novel TheraSilence™ RNA Program | Salus (Health) | Scoop.it

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.


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Krishan Maggon 's curator insight, May 24, 1:53 AM
Celsion Announces Potent, Durable Preclinical Lung Expression Data for Its Novel TheraSilence™ RNA ProgramCompany's First-in-Class Technology Enables Lung-Specific Delivery of RNA in Non-Human Primates
Therapeutic RNA Development Can Now Focus on Lung Disease
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PJ-34 inhibits PARP-1 expression and ERK phosphorylation in glioma-conditioned brain microvascular endothelial cells

PJ-34 inhibits PARP-1 expression and ERK phosphorylation in glioma-conditioned brain microvascular endothelial cells | Salus (Health) | Scoop.it

Abstract

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.

 


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Krishan Maggon 's curator insight, May 3, 6:05 AM

 

 

 

European Journal of Pharmacology

Available online 28 April 2015

In Press, Uncorrected Proof — Note to users

Molecular and cellular pharmacology PJ-34 inhibits PARP-1 expression and ERK phosphorylation in glioma-conditioned brain microvascular endothelial cellsCarla Mottaa, 1, Floriana D’Angelia, 1, Marina Scaliaa, Cristina Satrianob, Davide Barbagalloa, Irina Naletovaa, Carmelina Daniela Anfusoa, Gabriella Lupoa, Vittoria Spina-Purrelloa, ,   doi:10.1016/j.ejphar.2015.04.026
Rescooped by Pasquale Valente from Longevity science
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Personalized Devices Predict Cancer Drug Response | The Scientist Magazine®

Personalized Devices Predict Cancer Drug Response | The Scientist Magazine® | Salus (Health) | Scoop.it
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.

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Rescooped by Pasquale Valente from Bauer Physical Therapy(Bauer Health Action)
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Is this the purpose of sleep?

Is this the purpose of sleep? | Salus (Health) | Scoop.it
Despite massive scientific advancement in the last 50 years into our understanding of what sleep is and what it does for the body, the answer to the simple question, "what is the purpose of sleep,"...

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Randy Bauer's curator insight, April 13, 4:06 PM

The processes of sleep actively facilitate restoration of the mind and physical self for next-day functioning. 


Last year, a major paper was published in the journal Science describing how, during sleep, the brain removes waste products. Lead author, Lulu Xie, said:

 

“The restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake brain.”


https://youtu.be/MJK-dMlATmM

Rescooped by Pasquale Valente from The future of medicine and health
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Scientists create functioning "mini-lungs" to study cystic fibrosis

Scientists create functioning "mini-lungs" to study cystic fibrosis | Salus (Health) | Scoop.it
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.

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