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Newswise PHILADELPHIA Workhorse molecules called heat-shock proteins contribute to refolding proteins that were once misfolded and clumped, causing such disorders as Parkinson's disease, amyotrophic lateral sclerosis, and Alzheimer's disease. James Shorter, PhD, an associate professor of Biochemistry and Biophysics, at the Perelman School of Medicine at the University of Pennsylvania, has been developing ways to "reprogram" one such protein a yeast protein called Hsp104 -- to improve its therapeutic properties.

But precise knowledge about the mechanisms by which Hsp104 works to fix misshapened and clumped proteins has been lacking. Now, Shorter and his colleagues have discovered that a previously disregarded part of the Hsp104 structure, the N-terminal domain (NTD), located at one end of the Hsp104 molecule, is a major player in its protein-busting powers. Their work was published in Molecular Cell.

"We've defined in unprecedented detail the mechanism by which Hsp104 dissolves its natural substrate, Sup35 prions," says Shorter. "We found that the N-terminal domain of Hsp104 allows the enzyme to function in a way that enables the disintegration of the prion." Prions are infectious proteins that cause disease in humans, but can be beneficial in yeast.

While Hsp104 is found in the vast majority of less complex organisms on the planet, it was somehow lost in the evolution of lower forms of life to more complex animals and humans. It's baffling in many ways," says Shorter. "We don't understand quite why Hsp104 was lost. But it could be useful in a therapeutic setting because we could add back an activity that humans don't really have: the ability to rapidly dissolve and refold prions." Previously, Shorter and colleagues defined a set of human heat shock proteins that can slowly dissolve prions.

Although previous work by Shorter and others had shown that the middle section of Hsp104 was vital for its clump-busting activity, the N-terminal domain was thought to be relatively unimportant. "Researchers had thought it was a more dispensable domain," says lead author, Elizabeth Sweeny, PhD, a former graduate student in the Shorter lab who is now a postdoctoral fellow at the Massachusetts Institute of Technology. "We reveal in this paper that when you give Hsp104 a very difficult protein clump to break up, like those seen in neurodegenerative disease protein inclusions, it actually becomes very important."

Shorter and his collaborators used small-angle X-ray scattering (SAXS) to examine the role of the Hsp104 N-terminal domain by deleting it from the enzyme and testing it under different conditions. When Hsp104 lacking the NTD (Hsp104N) is introduced into the formation of the Sup35 prions in a test tube, it promoted prion formation, instead of solubilizing prions. The researchers also observed that, while Hsp104 attacks the Sup35 prion by breaking up the head and tail contacts that hold the prion together, Hsp104N was unable to do likewise. Hsp104N is able to dissolve disordered protein aggregates but cannot break down prions due to their increased stability.

Sweeny found that Hsp104 normally shaped like a short, hexagonal tube -- works like a peristaltic pump that shuttles molecules through its central channel. ATP, the cells energy molecule, is the fuel that powers the pump.

The altered structure of Hsp104N greatly impairs this normal mechanism, affecting its ability to break apart Sup35 and other prions. Sweeny notes, "Hsp104 extracts individual proteins from the prion fibril by pumping them through its central channel and that's how it dissolves them. The N-terminal domain of Hsp104 allows the enzyme to function in a more powerful way that enables dissolution of the very stable Sup35 yeast prion."

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Penn Study Uncovers Secrets of a Clump-Dissolving Protein

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Newswise PHILADELPHIAA somatic mutation in the ATRX gene has recently been shown as a potential molecular marker for aggressive brain tumors, such as gliomas, neuroblastomas and pancreatic neuroendocrine tumors. Now, for the first time, researchers at at the Perelman School of Medicine at the University of Pennsylvania have found that the same mutated gene may serve as a much-needed biomarker for the pheochromocytomas and paragangliomas (PCC/PGL) that become malignant. These rare neuroendocrine tumors are typically benign, but when they go rogue, they become very aggressive.

The study was published online ahead of print today in Nature Communications.

Several inherited mutated genes, such as VHL and RET, have been found to be associated with PCC/PGL; however, little is known about the somatic genetic changes leading to tumorigenesis in these patients.

This is the first step towards a better understanding of this type of disease, and to try to identify better biomarkers of poor outcomes, said senior author Katherine Nathanson, MD, an associate professor in the division of Translational Medicine and Chief Oncogenomics Physician for the Abramson Cancer Center. The mutation could not only serve as that biomarker for metastatic disease, but also a potential therapeutic drug target in the future.

PGLs are rare tumors of nerve ganglia in the body, whereas PCCs form in the center of the adrenal gland, which is responsible for producing adrenaline. The tumor causes the glands to overproduce adrenaline, leading to elevated blood pressure, severe headaches, and heart palpitations. Both are found in about two out of every million people each year. An even smaller percentage of those tumors become malignant. For that group, the five-year survival rate is about 50 percent.

No reliable predictors of aggressive disease exist other than an inherited mutation in the SDH gene, but only half of patients who develop metastatic disease carry that mutation, meaning the other half have no known predictors.

About 60 percent of PCC/PGLs are sporadic, while the remaining 40 percent are hereditary. Most recurrent somatic mutations are observed almost exclusively in sporadic PCC/PGLs.

Researchers, including Lauren Fishbein, MD, PhD, MTR, an instructor in the division of Endocrinology, Diabetes and Metabolism at the Perelman School of Medicine, investigated the mutations using whole exome sequencing on a set of 21 tumor/matched germline DNA samples of either sporadic or inherited PCC/PGL. The idea was to compare benign tumors to clinically aggressive ones in order to spot markers of malignant potential.

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Mutated ATRX Gene Linked to Brain and Pancreatic Neuroendocrine Tumors is Potential Biomarker for Rare Adrenal Tumors ...

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Newswise NORTHFIELD, ILL. The College of American Pathologists (CAP), the American Society of Clinical Oncologys (ASCO) ASCO University, and the Association for Molecular Pathology (AMP) recently announced their partnership in the creation of the Molecular Oncology Tumor Board series, an online and user-driven resource designed to help cancer care providers with the interpretation and understanding of tumor molecular profiling tests and studies.

The new crowd-sourced series allows for maximum user input and interaction, and encourages a multidisciplinary discussion of this rapidly growing area of cancer care. Access to the Molecular Oncology Tumor Boards is now available for free through the ASCO Connection website, ASCOConnection.org.

A healthy flow of information between oncologists and pathologists is critical to meeting each cancer patients unique goals and needs during treatment, said CAP President Gene N. Herbek, MD, FCAP. The Molecular Oncology Tumor Board series offers an education opportunity for pathologists and oncologists to share the latest information and best practices in genomic medicine in a convenient, real-time format.

Each month the Molecular Oncology Tumor Boards will feature a case-based discussion involving genetic or genomics in the treatment of cancer. The open forum will allow participants to post questions or comments about the cases, engage in discussion, and compare approaches.

Understanding the results of tumor molecular profiling studies is challenging, and the field of cancer genomics is rapidly changing with new information being generated at a dizzying pace, said ASCO Chief Medical Officer Richard L. Schilsky, MD, FACP, FASCO. All oncologists struggle to keep abreast of this information and to learn how to use tumor molecular profiling to deliver high-quality, personalized cancer care. We hope that this new educational program will foster learning about tumor molecular genomics in an engaging and interactive format fueled by real-world case studies.

Two rotating faculty members, a pathologist and medical oncologist, will lead the case discussion each month, provide input, and after two weeks of discussion, will post a summary of the case discussion that addresses actionable aberrations identified and treatment options available based on clinical parameters. The information provided in the case discussions are designed to be educational and are not intended to make treatment recommendations.

The Molecular Oncology Tumor Boards is available to anyone who creates an ASCO.org account and logs into ASCOConnection.org. Participants who complete and pass a short post-test can also earn Continuing Medical Education credit.

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CAP Partners to Launch Crowd-Sourced Molecular Oncology Tumor Board Series

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Newswise Case Western Reserve scientists have taken a huge leap toward identifying root causes of psoriasis, an inflammatory skin condition affecting 125 million people around the world. Of the roughly 50,000 proteins in the human body, researchers have zeroed in on four that appear most likely to contribute this chronic disease. The findings, published this month in Molecular & Cellular Proteomics, dramatically advance efforts to understand how psoriasis develops and, in turn, how to stop it.

Psoriasis affects 2 to 3 percent of the population worldwide, said senior author Nicole L. Ward, PhD, associate professor of dermatology and neurosciences, Case Western Reserve University School of Medicine. The underlying cause of psoriasis remains unknown, and the specific signals that trigger disease onset are still being investigated. There currently is no cure.

Wards lab is focused on studying the pathogenesis of the disease and its co-morbidities, including heart attack and stroke. Her group is actively working to identify new molecules key to the disease process that could become potential drug targets. Ward has a personal interest in this research her father suffers from psoriasis.

Psoriasis is an autoimmune skin disease characterized by well-demarcated areas of red, raised and scaly skin next to areas of normal-appearing skin. Autoimmune diseases are those where the body launches an abnormal immune response against its own tissues. Another complication of psoriasis is joint involvement, a condition termed psoriatic arthritis.

Ward and her team first narrowed their pool of potential culprits to about 1,280 proteins that are differentially regulated in the condition. From there, they focused on five that stood out either because of their high prevalence in human psoriasis or their prominence in other studies relating to human psoriasis tissue. Wards lab team took skin tissue samples from her well-established psoriasis transgenic mouse model, called the KC-Tie2 mouse, and compared it to skin tissue samples of normal mice. Her lab collaborated with Mark R. Chance, PhD, director of the Center for Proteomics and Bioinformatics, CWRU School of Medicine, and his team at the center to identify new proteins that were differentially regulated in the skin tissue of psoriasis mice compared to the skin tissue of healthy mice.

To ensure that the proteins identified in the mouse were important to human psoriasis, her team then examined human psoriasis skin cells, known as keratinocytes, and human psoriasis skin tissue samples to confirm the increased presence of these proteins in human disease. In the skin of the psoriasis mice, investigators first identified increases in stefin A1 (342.4-fold increased; called cystatin A in humans); slc25a5 (46.2-fold increased); serpinb3b (35.6-fold increased; called serpinB1 in humans) and KLK6 (4.7-fold increased). The team found no increases of the Rab18 protein in skin tissue of the mice, and so ruled it out as a psoriasis-generating culprit. Investigators then confirmed the increased presence of the Serpinb3b, KLK6, Stefin A1 and Slc25a5 proteins in human lesional psoriasis skin tissue, and human lesional psoriasis skin cells compared to healthy control skin tissue and skin cells.

We were interested in looking for the increased presence of these proteins, not just in the psoriasis-like skin inflammation of the mouse, but more importantly, we needed to know how the increased presence of these proteins translated to human psoriasis, Ward said. So we took the information we discovered in the mouse model and went back to the patients and confirmed the increase in these proteins in their lesional psoriasis skin tissue. We are really focused on, and enthusiastic about, our ability to perform successfully translational bench-to bedside-and-back-again psoriasis research here at CWRU School of Medicine Department of Dermatology and the Murdough Family Center for Psoriasis at University Hospitals Case Medical Center. Its what we excel at and what we love to do.

The next step in pursuing this line of research for Wards team will be uncovering the role and significance of each of these proteins in the progression of psoriasis. Determining the individual contributions of each protein will help provide strategic therapeutic targets to change the course of a patients psoriasis or, at the very least, provide a better understanding of how a change in the regulation of these proteins contributes to skin inflammation and psoriatic disease.

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Case Western Reserve Scientists Identify Proteins Likely to Trigger Psoriasis

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Newswise Researchers at the University of California, San Diego School of Medicine, with collaborators in Korea and Scotland, have identified a novel signaling pathway critical to the immune response of cells associated with the initiation of allergic asthma. The discovery, they say, could point the way to new therapies that suppress the inflammatory allergic response, offering potential relief to millions of Americans with the chronic lung condition and potentially other allergic diseases.

The results are published in the January 19 online Early Edition of the Proceedings of the National Academy of Sciences.

Specifically, the scientists demonstrated that T helper 2 (Th2) type inflammation in allergic asthma involves dendritic cells (DC), a type of white blood cell, which trigger a reduction in the production of cyclic AMP or cAMP, a key messenger molecule for signaling inside cells. In mouse models, deletion of the gene that codes for a protein that promotes the production of cAMP resulted in spontaneous bronchial asthma, which shares many similarities with human asthma. Conversely, increasing cAMP levels inhibited the cells inflammatory response that results in asthmas characteristic symptoms.

These findings and the related mechanism are very different from the current residing view of activation of specific T helper cell responses, said principal investigator Eyal Raz, MD, professor of medicine.

The role of cAMP formation and action in dendritic cells in the induction of allergic response was really surprising, added co-author Paul Insel, MD, professor of pharmacology and medicine. It suggested to us that this signaling pathway is involved in other immune-related functions.

The immune response of humans, mice and other vertebrates consists of two fundamental components. The first is the innate immune system, which recognizes and responds to pathogens in an immediate, but generalized, way and does not confer long-lasting immunity. The second is the adaptive immune system in which highly specialized T and B cells eliminate or prevent pathogen growth and create immunological memory in case of future encounters with the same pathogen.

Th2 immunity is one of two major aspects of adaptive immunity. Th1 responses target intracellular pathogens, such as viruses and bacteria that have invaded host cells. The Th2 response is more effective against extracellular pathogens (such as bacteria, parasites and toxins that operate outside of cells) and also plays a major role in allergic reactions and related diseases.

Allergic asthma is triggered by inhaled allergens, such as pet dander, pollen, mold and dust mites. It is characterized by inflammation and narrowing of the airways, resulting in wheezing, chest tightness, shortness of breath, coughing and other symptoms. The common form of allergic asthma is associated with an exaggerated Th2 immune response. Allergic asthma affects people of all ages, most often appearing in childhood. More than 25 million Americans suffer from the condition.

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New Cellular Pathway Triggering Allergic Asthma Response Identified

Somerset, Pennsylvania (PRWEB) January 15, 2015

In a recent announcement by Universal Forensics Corporation, company President and CEO, Julie Cramer, commented, "We are pleased and proud to make the appointment of Dr. Brian Reese to the position of Senior Scientist. Dr. Reese has an extensive background and experience in genetics and molecular medicine which will serve us and our industry well as we continually explore new methods to improve our DNA paternity and relationship testing protocols. We invite all of our distributor lab partners to get to know Dr. Reese and welcome him to our growing team of professionals."

Dr. Reese received his undergraduate degree in biology and chemistry from Allegheny College of Meadville, PA. and his doctorate degree from the prestigious Johns Hopkins University School of Medicine where he majored in molecular medicine. Dr. Reese also received a research fellowship from the University of Pittsburgh Drug Discovery Institute. Most recently, Dr. Reese served as a Technology Consultant with Thermo Fisher Scientific, one of the leading biotechnology companies in the United States. Dr. Reese and his wife, Amy, are natives of Western Pennsylvania and when asked about his new position with Universal Forensics, Brian commented, "My wife and I are thrilled for the opportunity and new challenge...we love the outdoors and all the recreational possibilities that Western Pennsylvania has to offer our family. We are so glad to be able to call this area home."

Universal Forensics Corp. is an accredited AABB (American Association of Blood Banks) laboratory headquartered in Somerset, Pennsylvania. Additional information can be obtained through the company website http://www.ufclab.com or by contacting services(at)ufclab(dot)com.

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Universal Forensics Corp. Announces the Appointment of Dr. Brian Reese to the Position of Senior Scientist

Researchers from Virginia Commonwealth University (VCU) Massey Cancer Center and the VCU Institute for Molecular Medicine (VIMM) have identified a new protein-protein interaction that could serve as a target for future therapies for the most common form of brain cancer, glioblastoma multiforme (GBM). GBM is a devastating disease that originates from glia or their precursors within the central nervous system, and the prognosis for GBM patients is unfortunately poor, but this discovery offers new therapeutic potential.

According to a new study recently published in the online edition of the journal Cancer Research, scientists pinpointed a novel interaction between the genes AEG-1 and Akt2 that regulates the malignant characteristics of GBM. Prior research by the study's lead author, Paul B. Fisher, M.Ph., Ph.D., discovered the AEG-1 gene and found it to be overexpressed in the vast majority of cancers. The Akt2 gene is also overexpressed in several additional cancers. This new research demonstrates a positive feedback loop between the proteins expressed by these genes that promote GBM growth and survival.

"This is the first time that this specific protein-protein signaling complex has been identified in GBM, and it gives us a new potential target for drug development," says Fisher, Thelma Newmeyer Corman Endowed Chair in Cancer Research and co-leader of the Cancer Molecular Genetics research program at VCU Massey, professor and chair of the Department of Human and Molecular Genetics at the VCU School of Medicine, and director of the VIMM. "If we can develop drugs that disrupt the interaction between these two proteins, we could potentially combine them with conventional therapies to more effectively treat malignant gliomas."

Cell signaling is a complex process where interactions between cells and their environment govern basic cellular functions and activities. Bin Hu, PhD, senior postdoctoral scientist on Fisher's team discovered that the interaction between the AEG-1 and Akt2 proteins was critical for further Akt2 signaling, which regulates tumor cell survival, proliferation and invasion.

Additionally, analyses of patient tissue samples showed that AEG-1 and Akt2 expression correlated with GBM progression and reduced patient survival. In preclinical experiments, the researchers disrupted AEG-1/Akt2 interaction through a process known as competitive binding and observed a reduction in GBM cell survival and invasion. When combined with AEG-1 silencing in mouse models of human GBM, there was a marked increase in survival.

"In this study we mapped the interacting regions in both genes in order to begin the process of developing drugs that can fill in these spaces and block the genes from binding," says Fisher. "If successful, these new treatments could also be applicable to a variety of additional cancers in which both genes are overexpressed."

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Fisher collaborated on this research with: Bin Hu, Ph.D., senior postdoctoral scientist in the VCU Department of Human and Molecular Genetics; Luni Emdad, M.B.B.S., Ph.D., member of the Cancer Molecular Genetics research program at Massey, assistant professor in the VCU Department of Human and Molecular Genetics and member of the VIMM; Devanand Sarkar, M.B.B.S., Ph.D., Harrison Scholar and member of the Cancer Molecular Genetics research program at Massey, Blick Scholar, associate professor in the VCU Department of Human and Molecular Genetics and associate scientific director, Cancer Therapeutics, in the VIMM; Swadesh K. Das, Ph.D., member of the Cancer Molecular Genetics research program at Massey, member of the VIMM and assistant professor in the VCU Department of Human and Molecular Genetics; Manny Bacolod, Ph.D., instructor in the VCU Department of Human and Molecular Genetics; Timothy P. Kegelman, graduate student in the M.D./Ph.D. program at VCU School of Medicine; and Mohammad Al-Zubi and Xue-Ning Shen, both research technicians in the VCU Department of Human and Molecular Genetics and the VIMM.

This study was supported by National Institutes of Health(NIH)-National Cancer Institute (NCI) grants R01 CA134721 and R01 CA138540; The National Foundation for Cancer Researcher; the James S. McDonnell Foundation; and, in part, by VCU Massey Cancer Center's NIH-NCI Cancer Center Support Grant P30 CA016059.

The full manuscript of this study is available online at: http://cancerres.aacrjournals.org/content/74/24/7321.long

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New target identified for potential brain cancer therapies

Dr. David Tamborero on the Landscape of Lesions in MM and Consequences for Targeted Drug Response
Landscape of Driver Lesions in Multiple Myeloma and Consequences for Targeted Drug Response David Tamborero, PhD Institute for Molecular Medicine Finland (FIMM) University of Helsinki Helsinki, ...

By: International Myeloma Foundation

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Dr. David Tamborero on the Landscape of Lesions in MM and Consequences for Targeted Drug Response - Video

NORTHFIELD, ILL. --The College of American Pathologists (CAP), the International Association for the Study of Lung Cancer (IASLC), and the Association for Molecular Pathology (AMP) are teaming to revise the evidence-based guideline, "Molecular Testing Guideline for Selection of Lung Cancer Patients for EGFR and ALK Tyrosine Kinase Inhibitors."

The updated guideline will include new recommendations for ALK testing by IHC, ALK-EGFR resistance, and a number of emerging target molecular targets which will include, but is not limited to, ROS1, MET, ERBB2, RET, NTRK1. Multiplexed "Next Generation Sequencing" multigene panels and the reassessment of immunohistochemistry will be reviewed. The role of rebiopsy and repeat analysis in the setting of post-treatment relapse, along with testing of blood samples for mutations in circulating tumor cells, cell free tumor DNA, or exosomes will be considered.

The revision of the guideline will again be based on evidence from unbiased review of published experimental literature. The revisions will be recommended by an expert panel made up of renowned worldwide leaders in the field. The revision will start in early 2015, taking around 18 months to complete. The three organizations collaborated in 2013 to develop the original version of the guideline which addressed which patients and samples should be tested and when and how testing should be performed.

"Although only one year has passed since the molecular testing guideline was published, rapid accumulation of scientific knowledge and new evidence in this field indicate that the guidelines should be updated. Thus, an update has begun that includes an expanded list of genes and new methods that are clinically relevant," said Yasushi Yatabe, MD, PhD, chief, Department of Pathology and Molecular Diagnostics, Aichi Cancer Center, Nagoya, Japan and IASLC member.

Patients battling lung cancer in the United States and abroad have continued hope with the benefits of these guidelines. Testing for the EGFR mutation and ALK rearrangements and the use of targeted therapies have given lung cancer patients the chance for survival, along with improved quality of life and time with loved ones.

"More than 224,200 new cases of lung cancer were diagnosed in 2014 in the United States," said Philip T. Cagle, MD, FCAP, medical director of Pulmonary Pathology in the Department of Pathology and Genomic Medicine at The Methodist Hospital in Houston, Texas, Archives of Pathology and Laboratory Medicine editor-in-chief, and CAP member. "Rapid advancements in genetic testing offer new treatment options for patients with advanced lung cancer. The updates to the guideline will help pathologists and oncologists to provide more accurate testing, leading to more optimal patient care."

As an active and asymptomatic recently retired, exceedingly proud new grandmother, Linda Wilkinson was completely taken aback by the diagnosis of Stage 4 lung cancer. She underwent three rounds of genomic testing and was identified as having the EML4-ALK translocation in June and has been on Xalkori since then with visible improvement in the shrinkage of her primary tumor.

No new metastases have been noted "I live in gratitude for all the professionals working in the area of genomic testing and targeted treatment. Since going on a targeted agent which specifically addresses my genetic mutation, I have felt renewed hope, energy and enthusiasm for life. It has lengthened my time horizon immensely and I foresee the day when these technologies (and new drug developments) make living with cancer something that can be successfully managed for years and years."

In an era of precision medicine, the guideline provides recommendations for pathologists, oncologists, and other cancer health professionals on the current state-of-the-art recommendations for the molecular testing of lung cancer.

"Molecular testing of the lung cancer patient's tumor is today crucial for selection the most optimal therapy from the treatment start", says Professor Fred R. Hirsch, MD, PhD, University of Colorado and CEO of the International Association for the Study of Lung Cancer (IASLC). "It is also necessary to address eventual molecular testing of tumors from patients, who eventually progress on first-line therapy in order to learn about biological mechanisms for treatment failure and for guiding subsequent therapy today and in the future," continues Dr. Hirsch.

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Revisions to molecular testing guideline continues to give hope to lung cancer patients

The Association for Molecular Pathology (AMP), the premier global, non-profit organization serving molecular testing professionals, announced the release of an important white paper addressing the consequences of regulatory and reimbursement forces directed against molecular diagnostic testing that threaten patient care. The paper, titled, "A Molecular Diagnostic Perfect Storm: The Convergence of Regulatory & Reimbursement Forces that Threaten Patient Access to Innovations in Genomic Medicine" is now available online at http://bit.ly/1yGlghJ.

"The breakthroughs made possible by mapping the human genome -- a multi-billion dollar project that took more than a decade to complete -- are being threatened by government regulations, which in turn are threatening patient access to truly revolutionary treatments," said Victoria M. Pratt, PhD, Indiana University School of Medicine, active AMP Member, and lead author of the paper. "We hope that this manuscript further enlightens regulatory and reimbursement stakeholders about the storm brewing in Washington that could dismantle the development and coverage of important molecular diagnostic tests."

Medical professionals in universities, cancer centers, clinical laboratories, and pharmaceutical/manufacturing companies across the country have honored the public trust in the Human Genome Project by developing hundreds of innovative diagnostic tests and therapies that are advancing modern medicine in ways that would have been impossible without this breakthrough. By eliminating the barriers outlined in "The Perfect Storm" paper, genome-based research will continue to play a critical role in the development of more powerful tools to treat complex diseases such as cancer, diabetes, and cardiovascular disease.

Threats stemming from efforts by the U.S. Food and Drug Administration (FDA) and the Centers for Medicare and Medicaid Services (CMS), the two federal agencies that oversee molecular diagnostic testing, are the cause of this "Perfect Storm."

The FDA's new policies will effectively reformulate existing medical device regulations and consider medical professionals as manufacturers which will impose substantially new and duplicative requirements on clinical laboratories and hospitals. Meanwhile, CMS, who runs Medicare, the nation's largest insurer and whose actions are frequently mimicked in the private sector, has taken a heavy handed approach in denying coverage or reducing payment for several medically necessary molecular pathology tests. Unfortunately, health care providers -- those developing and delivering innovative diagnostic tests -along with patients, who are the ultimate intended beneficiaries, are caught in the middle.

"AMP is addressing the consequences of this gathering perfect storm of regulatory and reimbursement challenges directed against molecular diagnostic testing with recommendations designed to preserve patient access to these essential medical services" said AMP President, Janina Longtine, MD. "We are greatly concerned that these forces are coalescing to bring about consolidation of laboratory testing, to the detriment of local testing. This would have far-reaching negative effects on the healthcare system. As such, AMP is committed to working with the regulatory and reimbursement bodies to find a resolution that optimizes patient safety and offers access to important medical tests."

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The above story is based on materials provided by Association for Molecular Pathology. Note: Materials may be edited for content and length.

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Convergence of regulatory, reimbursement forces threaten patient care, experts say

White paper examines the challenges to providing innovative care and emphasizes recommendations to mitigate potential harm to patients

The Association for Molecular Pathology (AMP), the premier global, non-profit organization serving molecular testing professionals, announced the release of an important white paper addressing the consequences of regulatory and reimbursement forces directed against molecular diagnostic testing that threaten patient care. The paper, titled, A Molecular Diagnostic Perfect Storm: The Convergence of Regulatory & Reimbursement Forces that Threaten Patient Access to Innovations in Genomic Medicine is now available online at http://bit.ly/1yGlghJ.

"The breakthroughs made possible by mapping the human genome - a multi-billion dollar project that took more than a decade to complete - are being threatened by government regulations, which in turn are threatening patient access to truly revolutionary treatments," said Victoria M. Pratt, PhD, Indiana University School of Medicine, active AMP Member, and lead author of the paper. "We hope that this manuscript further enlightens regulatory and reimbursement stakeholders about the storm brewing in Washington that could dismantle the development and coverage of important molecular diagnostic tests."

Medical professionals in universities, cancer centers, clinical laboratories, and pharmaceutical/manufacturing companies across the country have honored the public trust in the Human Genome Project by developing hundreds of innovative diagnostic tests and therapies that are advancing modern medicine in ways that would have been impossible without this breakthrough. By eliminating the barriers outlined in "The Perfect Storm" paper, genome-based research will continue to play a critical role in the development of more powerful tools to treat complex diseases such as cancer, diabetes, and cardiovascular disease.

Threats stemming from efforts by the U.S. Food and Drug Administration (FDA) and the Centers for Medicare and Medicaid Services (CMS), the two federal agencies that oversee molecular diagnostic testing, are the cause of this "Perfect Storm."

The FDA's new policies will effectively reformulate existing medical device regulations and consider medical professionals as manufacturers which will impose substantially new and duplicative requirements on clinical laboratories and hospitals. Meanwhile, CMS, who runs Medicare, the nation's largest insurer and whose actions are frequently mimicked in the private sector, has taken a heavy handed approach in denying coverage or reducing payment for several medically necessary molecular pathology tests. Unfortunately, health care providers - those developing and delivering innovative diagnostic tests -along with patients, who are the ultimate intended beneficiaries, are caught in the middle.

"AMP is addressing the consequences of this gathering perfect storm of regulatory and reimbursement challenges directed against molecular diagnostic testing with recommendations designed to preserve patient access to these essential medical services" said AMP President, Janina Longtine, MD. "We are greatly concerned that these forces are coalescing to bring about consolidation of laboratory testing, to the detriment of local testing. This would have far-reaching negative effects on the healthcare system. As such, AMP is committed to working with the regulatory and reimbursement bodies to find a resolution that optimizes patient safety and offers access to important medical tests."

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About the Association for Molecular Pathology

The Association for Molecular Pathology (AMP) was founded in 1995 to provide structure and leadership to what was, at the time, the newly?emerging field of molecular diagnostics. Through the efforts of its Board of Directors, Committees, Working Groups, and members, AMP has established itself as the primary resource for expertise, education, and collaboration on what is now one of the fastest growing fields in healthcare. AMP members influence policy and regulation on the national and international levels, ultimately serving to advance innovation in the field and protect patient access to high quality, appropriate testing.

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AMP releases 'A Molecular Diagnostic Perfect Storm' paper

New European Research grant for diabetes researcher Dr. Francesca Spagnoli of the MDC

Diabetes researcher Dr. Francesca Spagnoli of the Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch has been awarded an extra research grant from the European Research Council (ERC). This Proof-of-Concept (PoC) grant is endowed with 150,000 euros over a period of two years. It is designed for researchers who already hold an ERC grant in order to transform their research results into practical applications. Dr. Spagnoli was named one of 50 recipients of this grant in 2014. In 2009 she received a one million euro ERC Starting Grant for her research on reprogramming liver cells into pancreas cells. Now, after having identified a factor that converts murine liver cells into pancreas cells, she wants to investigate whether human liver cells can also be reprogrammed into insulin-producing cells.

Diabetes affects more than 350 million people worldwide. In these patients, the insulin-producing beta cells of the pancreas have been destroyed or are dysfunctional, causing blood glucose levels to rise. In individuals with type 1 diabetes, the beta cells have been destroyed due to a misguided response of the immune system. These people must inject insulin throughout their whole life. People with type 2 diabetes are not able to utilize insulin properly, but can be treated with a special diet and drugs. However, even in these individuals, beta cell-function may decline over time, so that they, too, may need to inject insulin.

Insulin replacement therapy, however, has adverse side effects. This is why physicians have been trying for a long time to transplant intact beta cells or whole pancreas organs, but with little success. According to Dr. Spagnoli, there are several reasons for this. One is a shortage of donors; another is that the transplanted organ or cells frequently do not function well. After five years the patients often need a new transplant or have to inject insulin again.

Therefore, researchers are now focusing on cell-based therapy, which in their view represents the most promising option. Different potential sources for new beta cells are currently being explored, including embryonic stem cells and other cell types. A particularly attractive therapeutic strategy is to convert liver cells of diabetic patients into functional pancreatic beta cells through reprogramming. "Both organs derive from the same region in the embryo, and both play an important role in metabolism and in blood glucose regulation," Dr. Spagnoli explained. "Moreover, they share a number of genes." Her research has led to the identification of a novel factor that converts mouse liver cells into pancreatic cells. With her ERC PoC grant she wants to extend these findings to human liver cells and assess whether this strategy may be exploited to develop a cell-based therapy for diabetes using a patient's own liver cells, a so-called autologous cell-based therapy. An application to patent Dr. Spagnoli's discovery has been filed at the European Patent Office in Munich.

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Contact: Barbara Bachtler Press Department Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch in the Helmholtz Association Robert-Rssle-Strae 10; 13125 Berlin; Germany Phone: +49 (0) 30 94 06 - 38 96 Fax: +49 (0) 30 94 06 - 38 33 e-mail: presse@mdc-berlin.de http://www.mdc-berlin.de/en

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Reprogramming liver cells into pancreas cells

Shirley, NY (PRWEB) January 06, 2015

Physical Medicine Biodex develops technology for advancing patient progress, addressing the weak or balance deficient. The rehabilitation technology addresses neuromuscular evaluation, therapeutic exercise, gait training and range of motion difficulties in patients suffering from Stroke, Parkinson's disease, Spinal Cord and Traumatic Brain Injury, Orthopedic afflictions and Vestibular issues.

Biodex Medical Systems series of rehabilitation devices includes the Multi-Joint System 4 Dynamometer, Balance System SD, BioStep Semi-Recumbent Elliptical, Gait Trainer 3 and Unweighing System. These devices can be applied to neurorehabilitation, sports and orthopedic medicine, senior rehabilitation, and wellness.

To support the products, Biodex offers programs and protocols for specific applications including fall risk screening and conditioning and balance assessment for concussion management.

Nuclear Medicine and Molecular Imaging Biodex Medical Systems manufactures and distributes radiation shielding, protection and detection products for nuclear medicine, molecular imaging and radiation safety. Product offerings include dose calibrators, thyroid uptake, radiopharmaceutical chromatography, lung ventilation, exposure protection, cleanroom solutions, syringe shields, lead-lined cabinets, PET shipping systems and products to improve the image and procedure.

Medical Imaging Biodex offers surgical C-Arm Tables for pain care, cardiovascular and urologic procedures and Ultrasound Tables designed for echocardiography, OB/GYN and other general procedures. Both lines of tables are designed with ergonomic advances for the safety and comfort of both the sonographer and patient.

In addition, Biodex manufactures personal radiation protection. All Clear-Lead barriers are designed for imaging procedures using ionizing radiation, offering durable shatter resistant protection wherever its needed. The new Clear-Lead Personal Barrier is an adjustable height, lightweight barrier with convenient hour-glass design for hands-on access. The Mobile X-Ray barriers require little effort to maneuver and have a sleek, easy to clean design.

Visit Biodex booth # Z4AC17 for more information about all Biodex devices and products. Arab Health takes place January 26 - 29, 2015 at the Dubai International Convention & Exhibition Centre, Dubai.

If you are unable to attend the meeting and want to learn more about Biodex products, contact us directly at 1 800-224-6339 (Intl 631-924-9000), visit our website, http://www.biodex.com, or email us at info(at)biodex(dot)com.

About Biodex Medical Systems, Inc. Biodex Medical Systems, Inc. manufactures and distributes medical devices for physical medicine, nuclear medicine and molecular imaging, and medical imaging applications. It also provides concussion management as well as fall risk screening and conditioning programs. The Biodex commitment to innovative excellence spans more than 60 years. Our customer-driven support is why leading medical facilities around the globe call Biodex first.

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Biodex Medical Systems, Inc. Exhibiting at Arab Health 2015

DENVER - Implementation of molecular profiling is essential for the multidisciplinary team to effectively manage and care for non-small cell lung cancer (NSCLC) patients now and well into the future.

The International Association for the Study of Lung Cancer (IASLC) education teams will travel to various geographical locations within their regions in order to teach others the importance of and how to implement molecular testing using small group interactive learning sessions and hands-on approaches. The educational team will consist of medical oncologists, surgeons, pulmonologists, interventional radiologists, pathologists, nurses, laboratory personnel, molecular biologists, cytogeneticists, bioinformaticists and other scientists.

Lung cancer is the leading cause of cancer mortality for both men and women in the US and worldwide. Grouping all lung cancers together is no longer adequate for treatment-based decisions. Personalized medicine, treating the patient with therapies that are predicted to be effective based on the molecular characteristics of the tumor, can add years of life for those patients whose tumor harbor specific abnormalities and treated with a therapy specifically targeting this abnormality. Advanced-stage NSCLC patients with EGFR mutations or ALK rearrangements have a high response rate and increased progression-free survival when treated 1st-line with EGFR or ALK inhibitors, respectively, and within these categories there are approved agents. Testing for these two genomic alterations is now considered the standard of care for advanced-stage NSCLC. Additionally, these is a growing body of evidence from that supports the testing for other molecular aberrations (e.g. ROS1, BRAF, FGFR1, HER2, PIK3CA, MET and KRAS) as these are thought to be the oncogenic drivers of NSCLC and will be sensitive to therapies targeting these abnormalities.

The goal of IASLC's new program is to educate the multidisciplinary team on:

"About 225,000 new cases of lung cancer are diagnosed in the US every year. Molecular profiling of tumors from patients with lung cancer is crucial today for selecting the most optimal therapy," states Professor Fred R. Hirsch, MD, PhD, University of Colorado and CEO of IASLC. "IASLC is a global academic organization with a main focus of education for the lung cancer community, e. g. doctors, nurses, allied health personnel and the patients, about the most updated scientific knowledge and the standard of care for patients with lung cancer. This program is an important contribution to meet that goal, and we hope this program will reach many care-takers dealing with lung cancer, both in academic centers and in the communities."

"The IASLC has been on the forefront of promoting research and education related to lung cancer for over four decades," states Dr. Suresh Ramalingam, Chair of the IASLC Education Committee. "The overarching goal of this initiative is to ensure that every patient with lung cancer undergoes molecular testing according to the most recent guidelines in order to maximize clinical outcomes."

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About the IASLC:

The International Association for the Study of Lung Cancer (IASLC) is the only global organization dedicated to the study of lung cancer. Founded in 1974, the association's membership includes more than 4,000 lung cancer specialists in 80 countries. To learn more about IASLC please visit http://www.iaslc.org

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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IASLC announces it will conduct multidisciplinary live education programs for molecular profiling lung cancer in 2015

What does molecular medicine mean?
What does molecular medicine mean? A spoken definition of molecular medicine. Intro Sound: Typewriter - Tamskp Licensed under CC:BA 3.0 Outro Music: Groove G...

By: What Does That Mean?

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What does molecular medicine mean? - Video

HEIDELBERG, 30 December 2014 - Researchers in the United States have identified a molecular network that comprises many of the genes previously shown to contribute to autism spectrum disorders. The findings provide a map of some of the crucial protein interactions that contribute to autism and will help uncover novel candidate genes for the disease. The results are published in Molecular Systems Biology.

"The study of autism disorders is extremely challenging due to the large number of clinical mutations that occur in hundreds of different human genes associated with autism," says Michael Snyder, Professor at the Stanford Center for Genomics and Personalized Medicine and the lead author of the study. "We therefore wanted to see to what extent shared molecular pathways are perturbed by the diverse set of mutations linked to autism in the hope of distilling tractable information that would benefit future studies."

The researchers generated their interactome - the whole set of interactions within a cell - using the BioGrid database of protein and genetic interactions. "We have identified a specific module within this interactome that comprises 119 proteins and which shows a very strong enrichment for autism genes," remarks Snyder.

Gene expression data and genome sequencing were used to identify the protein interaction module with members strongly enriched for known autism genes. The sequencing of the genomes of 25 patients confirmed the involvement of the module in autism; the candidate genes for autism present in the module were also found in a larger group of more than 500 patients that were analyzed by exome sequencing. The expression of genes in the module was examined using the Allen Human Brain Atlas. The researchers revealed the role of the corpus callosum and oligodendrocyte cells in the brain as important contributors to autism spectrum disorders using genome sequencing, RNA sequencing, antibody staining and functional genomic evidence.

"Much of today's research on autism is focused on the study of neurons and now our study has also revealed that oligodendrocytes are also implicated in this disease," says Jingjing Li, Postdoctoral Fellow at the Stanford Center for Genomics and Personalized Medicine who helped to spearhead the work. "In the future, we need to study how the interplay between different types of brain cells or different regions of the brain contribute to this disease."

"The module we identified which is enriched in autism genes had two distinct components," says Snyder. "One of these components was expressed throughout different regions of the brain. The second component had enhanced molecular expression in the corpus callosum. Both components of the network interacted extensively with each other."

The working hypothesis of the scientists, which is consistent with other recent findings, is that disruptions in parts of the corpus callosum interfere with the circuitry that connects the two hemispheres of the brain. This likely gives rise to the different phenotypes of autism that result due to impairment of signaling between the two halves of the brain.

"Our study highlights the importance of building integrative models to study complex human diseases," says Snyder. "The use of biological networks allowed us to superimpose clinical mutations for autism onto specific disease-related pathways. This helps finding the needles in the haystack worthy of further investigation and provides a framework to uncover functional models for other diseases."

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Integrated systems analysis reveals a molecular network underlying autism spectrum disorders

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Molecular network identified underlying autism spectrum disorders

HEIDELBERG, 30 December 2014 - The outbreak of the Ebola virus disease occurring in West Africa may have originated from contact between humans and virus-infected bats, suggests a study led by researchers from the Robert Koch-Institute in Berlin, Germany. The report, published in EMBO Molecular Medicine, identifies insectivorous free-tailed bats as plausible reservoirs and expands the range of possible Ebola virus sources to this type of bats. The results also reveal that larger wildlife are not the source of infection.

Ebola virus disease epidemics are of zoonotic origin, transmitted to human populations either through contact with larger wildlife or by direct contact with bats. "We monitored the large mammal populations close to the index village Meliandou in south-eastern Guinea and found no evidence for a concurrent outbreak," says Fabian H. Leendertz of the Robert Koch Institute, who led the study. The second infection route appears more plausible as direct contact with bats is usual in the affected region.

Fruit bats are the commonly suspected Ebola virus reservoir as previous outbreaks in Africa show. Interviews with Meliandou locals revealed that exposure to fruit bats through hunting and consumption of meat in this area is common. Yet fruit bats seem an unlikely source of infection, as a food-borne transmission would have affected adults before or concurrently with the two-year-old boy - the index case. This suggests a source of infection unrelated to food.

Another opportunity for infection was a large colony of free-tailed insectivorous bats housed in a hollow tree nearby the home of the index case. Villagers reported that children often used to play in and around the tree. This may have resulted in a massive exposure to bats.

The multidisciplinary team of researchers led a four-week field mission in Guinea in April 2014 to examine human exposure to bats, to survey local wildlife and to capture and sample bats in Meliandou and in neighbouring forests. The index village is not located in the forest but rather in an area heavily modified by humans representing "modern" African settings.

The virus that spread from Meliandou into other areas of Guinea and Sierra Leone, Liberia, Nigeria and Senegal, represents the largest ever-recorded Ebola outbreak killing 7,800 people (as of 17 December 2014).

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Investigating the Zoonotic Origin of the West African Ebola Epidemic

Almudena Mar Saz, Sabrina Weiss, Kathrin Nowak, Vincent Lapeyre, Fee Zimmermann, Ariane Dx, Hjalmar S. Khl, Moussa Kaba, Sebastien Regnaut, Kevin Merkel, Andreas Sachse, Ulla Thiesen, Lili Villnyi, Christophe Boesch, Piotr W. Dabrowski, Aleksandar Radoni?, Andreas Nitsche, Siv Aina J. Leendertz, Stefan Petterson, Stephan Becker, Verena Krhling, Emmanuel Couacy-Hymann, Chantal Akoua-Koffi, Natalie Weber, Lars Schaade, Jakob Fahr, Matthias Borchert, Jan F. Gogarten, Sbastien Calvignac-Spencer, Fabian H. Leendertz

Read the paper: http://embomolmed.embopress.org/content/early/2014/12/29/emmm.201404792

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Bats are a possible source of the Ebola epidemic in West Africa

Published December 30, 2014

U.S. scientists have identified a molecular network of genes known to contribute to autism spectrum disorders, and they say their finding may help uncover new genes linked to these conditions.

"The study of autism disorders is extremely challenging due to the large number of clinical mutations that occur in hundreds of different human genes associated with autism," study author Michael Snyder, genetics and personalized medicine professor at Stanford University, said in a news release. "We therefore wanted to see to what extent shared molecular pathways are perturbed by the diverse set of mutations linked to autism in the hope of distilling tractable information that would benefit future studies."

According to the news release, researchers used gene expression data and genome sequencing to study the whole set of interactions within a cell, and they identified a module comprised of 119 proteins linked to autism genes.

The sequencing of the genomes was present in 25 study participants who had been diagnosed with autism, which confirmed the involvement of the module in autism. The autism candidate genes in the module were also present in more than 500 diagnosed patients who were analyzed by exome sequencing.

Researchers also found that the corpus callosum and oligodendrocyte cells in the brain can contribute to autism. Oligodendrocytes are myelin-forming cells of the central nervous system, and the corpus callosum is a huge band of myelinated fibers. Myelin, which is comprised of proteins and phospholipids, forms a sheath around nerve fibers and increases the speed at which impulses are conducted.

"In the future, we need to study how the interplay between different types of brain cells or different regions of the brain contribute to this disease, study author Jingjing Li, postdoctoral fellow at the Stanford Center for Genomics and Personalized Medicine, said in the news release.

Snyder said the module enriched in autism had two distinct components that exclusively interacted with each other: one that was expressed throughout different regions of the brain, and another that had enhanced molecular expression in the corpus callosum.

Based on their findings, the study authors hypothesized that disruptions in parts of the corpus callosum interfere with the circuitry that connects the two hemispheres of the brain, resulting in autism.

"Our study highlights the importance of building integrative models to study complex human diseases," Snyder said.

Read more here:

US researchers identify gene network linked to autism

Ebola "patient zero" may have been infected with the virus while playing with bats in a hollow tree in his village in Guinea, like the one seen at far left in this photo. EMBO Molecular Medicine

Where and how did the deadly Ebola outbreak begin? The disease that's killed more than 7,800 people across West Africa may have taken hold after a chance encounter last winter between a 2-year-old boy and wild bat in a hollowed-out tree.

New research published Tuesday in the journal EMBO Molecular Medicine provides an almost cinematic theory about the origins of the current Ebola outbreak, and also offers new evidence that a certain type of bat may play host to the deadly virus.

The study traces the activities of Ebola "patient zero," a 2-year-old boy in Mliandou, Guinea, who's believed to have been the virus' first victim in December 2013.

The researchers visited the village and neighboring areas, and learned from the residents that children liked to play in a hollow tree that was home to insect-eating free-tailed bats (Mops condylurus). These large fruit bats migrate annually to southeastern Guinea to the region of Klma, where Mliandou is located.

Previously, experts suspected that bush meat hunted and consumed by villagers might be the source of transmission. But the researchers say the child's father was not a hunter, and they did not find evidence that larger mammals were associated with the spread of the virus.

"In contrast, bat hunting was commonly described in the region," the researchers write. "Men of Meliandou and six other neighboring villages reported opportunistically hunting fruit bats throughout the year. Insectivorous bats were reported to be commonly found under the roofs of houses and similar hides in the villages. These bats are reportedly targeted by children, who regularly hunt and grill them over small fires."

Top, the village of Meliandou in Guinea, where a 2-year-old boy -- Ebola "patient zero" -- contracted the virus and died. Images below are of a hollow tree, a popular place where village children play. These trees frequently harbor insect-biting bats.

EMBO Molecular Medicine

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Encounter with bat may have sparked Ebola outbreak

December 23, 2014

A picture of a membrane protein called cysZ determined with Phenix software using data that could not previously be analyzed. (Credit: LANL)

Brett Smith for redOrbit.com Your Universe Online

Tiny molecular machines are expected to play a major role be the next generation of medicine as researchers at Los Alamos National Laboratory (LANL) in New Mexico have announced a new technique that allows for the first-ever 3D imaging of these miniscule machines, according to a report in the journal Nature Methods.

Inside each cell in our bodies and inside every bacterium and virus are tiny but complex protein molecules thatsynthesize chemicals, replicate genetic material, turn each other on and off, and transport chemicals acrosscell membranes, said Tom Terwilliger, a Los Alamos National Laboratory scientist. Understanding how all these machines work is the key to developing new therapeutics, fortreating genetic disorders, and for developing new ways to make useful materials.

Past research on molecular machines has taken advantage of the fact that any incorporated metal atoms diffract X-rays differently than a machines other atoms, which are typically carbon, hydrogen, nitrogen and oxygen. Computers could be used to seize on these differences and any machines without metal atoms had to be studied by incorporating metal into them.

Through the newly developed imaging method, the LANL team was able to show that robust statistical procedures might be used to locate metal atoms in molecular machines even if they dont spread X-rays differently than carbon and other atoms. The technique allows for metal atoms like sulfur, normally part of many proteins, to be discovered and used to produce a three-dimensional image of a protein. Also, the new technique makes it easy to see a three-dimensional image of a protein without unnaturally integrating metal atoms into them, which means a lot more molecular machines can be analyzed.

The updated procedure starts with scientists generating billions of copies of a particular protein machine, dissolving them in water and growing crystals of the protein. Next, the scientists aim a stream of X-rays at a crystal and assess the brilliance of all of the thousands of diffracted X-ray spots that are generated. Then, scientists use a software program called Phenix to assess the diffraction spots and generate a three-dimensional image of an individual protein machine. This image shows the scientists just how the protein machine is assembled.

One such machine that was recently investigated was the Cascade machine, which happens to be in bacteria and is used to identify DNA that comes from viruses that infect bacteria. Looking somewhat like a seahorse, Cascade is composed of 11 proteins and an RNA molecule, with the RNA molecule winding through the entire body of the seahorse. If a bit of foreign DNA is able to interlock with the RNA molecule, Cascade hold the foreign viral DNA in place as a different machine comes by and destroys it, keeping the bacterium from infection. A report on Cascade was published in the journal Science over the summer.

In addition to investigating Cascade, the Phenixsoftware has allowed scientists to determine three-dimensional configurations of more than 15,000 different protein machinesand has already been cited by more than 5000 scientific publications.

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First-ever 3D images of "molecular machines" produced