Global Web Analytics Market 2020-2024 | 19% CAGR Projection Over the Next Five Years | Technavio – Business Wire

LONDON--(BUSINESS WIRE)--The web analytics market size is poised to grow at a CAGR of over 19% during the period 2020-2024, according to the latest market research report by Technavio. Request a free sample report

The e-commerce industry is constantly evolving with the advent of new technologies and services. In addition, vendors are engaging in advanced marketing tactics to gain popularity and attract more customers. Consumer demand for personalized experiences, good services, and easy access to product information is also on the rise. Thus, enterprises that operate through e-commerce platforms analyze data collected from the websites to enhance website performance. The integration of web analytics helps online retailers to better understand consumer preferences by collecting information about website visitors so as to offer the right product offerings. Thus, the rising preference for online shopping will drive the web analytics market growth during the forecast period.

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As per Technavio, the proliferation of AI in web analytics will have a positive impact on the market and contribute to its growth significantly over the forecast period. This research report also analyzes other important trends and market drivers that will affect market growth over 2020-2024.

Web Analytics Market: Proliferation of AI in Web Analytics

Vendors in the market are increasingly integrating artificial intelligence (AI) into web analytics, which can provide more processed information from websites and makes web analytics more convenient for online marketers and website holders. Furthermore, machine learning helps in studying the patterns of human behavior on websites and can be correlated and analyzed with web analytics tools to find the desired result. Thus, the benefits of integrating AI into web analytics will prompt enterprises to adopt web analytics during the forecast period.

Other factors such as the growing need for predictive analytics, and the increasing adoption of the cloud will have a significant impact on the growth of the web analytics market value during the forecast period, says a senior analyst at Technavio.

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Web Analytics Market: Segmentation Analysis

This market research report segments the web analytics market by deployment (cloud-based and on-premises) and geography (APAC, North America, Europe, South America, and MEA).

The North American region led the market in 2019, followed by Europe, APAC, South America, and MEA respectively. The growth of the web analytics market share in North America can be attributed to factors such as the rising adoption of cloud computing services and the presence of various leading vendors in the region.

Technavios sample reports are free of charge and contain multiple sections of the report, such as the market size and forecast, drivers, challenges, trends, and more.

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Some of the key topics covered in the report include:

Market Landscape

Market Sizing

Five Forces Analysis

Market Segmentation

Geographical Segmentation

Market Drivers

Market Challenges

Market Trends

Vendor Landscape

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Global Web Analytics Market 2020-2024 | 19% CAGR Projection Over the Next Five Years | Technavio - Business Wire

The Brain, the Criminal and the Courts – TheFix.com

On March 30, 1981, 25-year-old John W. Hinckley Jr. shot President Ronald Reagan and three other people. The following year, he went on trial for his crimes.

Defense attorneys argued that Hinckley was insane, and they pointed to a trove of evidence to back their claim. Their client had a history of behavioral problems. He was obsessed with the actress Jodie Foster, and devised a plan to assassinate a president to impress her. He hounded Jimmy Carter. Then he targeted Reagan.

In a controversial courtroom twist, Hinckleys defense team also introduced scientific evidence: a computerized axial tomography (CAT) scan that suggested their client had a shrunken, or atrophied, brain. Initially, the judge didnt want to allow it. The scan didnt prove that Hinckley had schizophrenia, experts said but this sort of brain atrophy was more common among schizophrenics than among the general population.

It helped convince the jury to find Hinckley not responsible by reason of insanity.

Nearly 40 years later, the neuroscience that influenced Hinckleys trial has advanced by leaps and bounds particularly because of improvements in magnetic resonance imaging (MRI) and the invention of functional magnetic resonance imaging (fMRI), which lets scientists look at blood flows and oxygenation in the brain without hurting it. Today neuroscientists can see what happens in the brain when a subject recognizes a loved one, experiences failure, or feels pain.

Despite this explosion in neuroscience knowledge, and notwithstanding Hinckleys successful defense, neurolaw hasnt had a tremendous impact on the courts yet. But it is coming. Attorneys working civil cases introduce brain imaging ever more routinely to argue that a client has or has not been injured. Criminal attorneys, too, sometimes argue that a brain condition mitigates a clients responsibility. Lawyers and judges are participating in continuing education programs to learn about brain anatomy and what MRIs and EEGs and all those other brain tests actually show.

Most of these lawyers and judges want to know such things as whether brain imaging could establish a defendants mental age, supply more dependable lie-detection tests or reveal conclusively when someone is experiencing pain and when they are malingering (which would help resolve personal injury cases). Neuroscience researchers arent there yet, but they are working hard to unearth correlations that might help looking to see which parts of the brain engage in a host of situations.

Progress has been incremental but steady. Though neuroscience in the courts remains rare, were seeing way more of it in the courts than we used to, says Judge Morris B. Hoffman, of Colorados 2nd Judicial District Court. And I think thats going to continue.

Criminal law has looked to the human mind and mental states since the seventeenth century, says legal scholar Deborah Denno of Fordham University School of Law. In earlier centuries, courts blamed aberrant behavior on the devil and only later, starting in the early twentieth century, did they begin recognizing cognitive deficits and psychological diagnoses made through Freudian analysis and other approaches.

Neuroscience represents a tantalizing next step: evidence directly concerned with the physical state of the brain and its quantifiable functions.

There is no systematic count of all the cases, civil and criminal, in which neuroscientific evidence such as brain scans has been introduced. Its almost certainly most common in civil cases, says Kent Kiehl, a neuroscientist at the University of New Mexico and a principal investigator at the nonprofit Mind Research Network, which focuses on applying neuroimaging to the study of mental illness. In civil proceedings, says Kiehl, who frequently consults with attorneys to help them understand neuroimaging science, MRIs are common if theres a question of brain injury, and a significant judgment at stake.

In criminal courts, MRIs are most often used to assess brain injury or trauma in capital cases (eligible for the death penalty) to ensure that theres not something obviously neurologically wrong, which could alter the trajectory of the case, Kiehl says. If a murder defendants brain scan reveals a tumor in the frontal lobe, for instance, or evidence of frontotemporal dementia, that could inject just enough doubt to make it hard for a court to arrive at a guilty verdict (as brain atrophy did during Hinckleys trial). But these tests are expensive.

Some scholars have tried to quantify how often neuroscience has been used in criminal cases. A 2015 analysis by Denno identified 800 neuroscience-involved criminal cases over a 20-year period. It also found increases in the use of brain evidence year over year, as did a 2016 study by Nita Farahany, a legal scholar and ethicist at Duke University.

Farahanys latest count, detailed in an article about neurolaw she coauthored in the Annual Review of Criminology, found more than 2,800 recorded legal opinions between 2005 and 2015 where criminal defendants in the US had used neuroscience everything from medical records to neuropsychological testing to brain scans as part of their defense. About 20 percent of defendants who presented neuroscientific evidence got some favorable outcome, be it a more generous deadline to file paperwork, a new hearing or a reversal.

But even the best studies like these include only reported cases, which represent a tiny, tiny fraction of trials, says Owen Jones, a scholar of law and biological sciences at Vanderbilt University. (Jones also directs the MacArthur Foundation Research Network on Law and Neuroscience, which partners neuroscientists and legal scholars to do neurolaw research and help the legal system navigate the science.) Most cases, he says, result in plea agreements or settlements and never make it to trial, and theres no feasible way to track how neuroscience is used in those instances.

Even as some lawyers are already introducing neuroscience into legal proceedings, researchers are trying to help the legal system separate the wheat from the chaff, through brain-scanning experiments and legal analysis. These help to identify where and how neuroscience can and cant be helpful. The work is incremental, but is steadily marching ahead.

One MacArthur network team at Stanford, led by neuroscientist Anthony Wagner, has looked at ways to use machine learning (a form of artificial intelligence) to analyze fMRI scans to identify when someone is looking at photos they recognize as being from their own lives. Test subjects were placed in a scanner and shown a series of pictures, some collected from cameras they had been wearing around their own necks, others collected from cameras worn by others.

Tracking changes in oxygenation to follow patterns in blood flow a proxy for where neurons are firing more frequently the teams machine-learning algorithms correctly identified whether subjects were viewing images from their own lives, or someone elses, more than 90 percent of the time.

Its a proof of concept, at this stage, but in theory its a biomarker of recognition, Jones says. You could imagine that could have a lot of different legal implications such as one day helping to assess the accuracy and reliability of eyewitness memory.

Other researchers are using fMRI to try to identify differences in the brain between a knowing state of mind and a reckless state of mind, important legal concepts that can have powerful effects on the severity of criminal sentences.

To explore the question, Gideon Yaffe of the Yale Law School, neuroscientist Read Montague of Virginia Tech and colleagues used fMRI to brain-scan study participants as they considered whether to carry a suitcase through a checkpoint. All were told with varying degrees of certainty that the case might contain contraband. Those informed that there was 100 percent certainty that they were carrying contraband were deemed to be in a knowing state of mind; those given a lower level of certainty were classified as being in the laws definition of a reckless state of mind. Using machine-learning algorithms to read fMRI scans, the scientists could reliably distinguish between the two states.

Neuroscientists also hope to better understand the biological correlates of recidivism Kiehl, for instance, has analyzed thousands of fMRI and structural MRI scans of inmates in high-security prisons in the US in order to tell whether the brains of people who committed or were arrested for new crimes look different than the brains of people who werent. Getting a sense of an offenders likelihood of committing a new crime in the future is crucial to successful rehabilitation of prisoners, he says.

Others are studying the concept of mental age. A team led by Yale and Weill Cornell Medical College neuroscientist B.J. Casey used fMRI to look at whether, in differing circumstances, young adults brains function more like minors brains or more like those of older adults and discovered that it often depended on emotional state. Greater insight into the brains maturation process could have relevance for juvenile justice reform, neurolaw scholars say, and for how we treat young adults, who are in a transitional period.

It remains to be seen if all this research will yield actionable results. In 2018, Hoffman, who has been a leader in neurolaw research, wrote a paper discussing potential breakthroughs and dividing them into three categories: near term, long term and never happening. He predicted that neuroscientists are likely to improve existing tools for chronic pain detection in the near future, and in the next 10 to 50 years he believes theyll reliably be able to detect memories and lies, and to determine brain maturity.

But brain science will never gain a full understanding of addiction, he suggested, or lead courts to abandon notions of responsibility or free will (a prospect that gives many philosophers and legal scholars pause).

Many realize that no matter how good neuroscientists get at teasing out the links between brain biology and human behavior, applying neuroscientific evidence to the law will always be tricky. One concern is that brain studies ordered after the fact may not shed light on a defendants motivations and behavior at the time a crime was committed which is what matters in court. Another concern is that studies of how an average brain works do not always provide reliable information on how a specific individuals brain works.

The most important question is whether the evidence is legally relevant. That is, does it help answer a precise legal question? says Stephen J. Morse, a scholar of law and psychiatry at the University of Pennsylvania. He is in the camp who believe that neuroscience will never revolutionize the law, because actions speak louder than images, and that in a legal setting, if there is a disjunct between what the neuroscience shows and what the behavior shows, youve got to believe the behavior. He worries about the prospect of neurohype, and attorneys who overstate the scientific evidence.

Some say that neuroscience wont change the fundamental problems the law concerns itself with the giant questions that weve been asking each other for 2,000 years, as Hoffman puts it questions about the nature of human responsibility, or the purpose of punishment.

But in day-to-day courtroom life, such big-picture, philosophical worries might not matter, Kiehl says.

If there are two or three papers that support that the evidence has a sound scientific basis, published in good journals, by reputable academics, then lawyers are going to want to use it.

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.

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The Brain, the Criminal and the Courts - TheFix.com

The new CEO overseeing The Guardian has a Ph.D. in cell biology and neuroscience – Nieman Journalism Lab at Harvard

The Guardian has a new business-side leader: Annette Thomas, a veteran of the academic publishing world, will assume the role of CEO of Guardian Media Group in March.

When she does, she may well be the only head of a major media company to also have a Ph.D. in cell biology and neuroscience.

Thomas might seem to lack experience in the traditional news business, but shes been highly successful in scientific publishing, which has seen its own share of digital transformation in the past two decades. After grad school, she began as an editor at the journal Nature and stayed at its parent company, MacMillan Publishing, in various roles for 23 years, the last nine of them as CEO, overseeing its merger with Springer Nature. (Macmillan Publishing also included more consumer-facing publications, notably Scientific American.) Most recently, she was chief executive of Web of Science Group, a data, analytics, and software business focused on research and higher education that is part of Clarivate Analytics. She serves on the boards of Yale and Cambridge University Press.

Per The Guardian:

Neil Berkett, the chair of the GMG board, which made the appointment, said Thomas was well-equipped to deal with the challenges ahead. He said: Our journalism has had a stellar 12 months, and remains world class. Even so, its clear that well continue to face big headwinds in the global media sector in 2020 and beyond.

Her track record is exceptional she has consistently delivered sustainable growth through deep engagement with end-users, championing innovative new business models with more open access to content and data, and building diverse and inclusive management teams.

Her role was previously filled by David Pemsel, who announced last year he was leaving to become CEO of the English Premier League. (He ended up resigning from that role before he ever started after sexual harassment claims surfaced from his time at The Guardian.) At Guardian Media Group, he was making 706,000 a year ($917,492); todays announcement doesnt disclose Thomas salary.

Thomas appointment means that both the editorial and business sides of The Guardian are led by women. (Katharine Viner became editor in 2015.) And Thomas, who is of African-American and German descent, has now reached a level of power that few women of color have in the news business.

If youre looking to learn more about Thomas, heres an interview she did while CEO of Macmillan in 2011, and here are two talks she gave in 2018 while at Clarivate, the second on The Future of Research Information: Open, Connected, Seamless.

You can find the full announcement here.

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The new CEO overseeing The Guardian has a Ph.D. in cell biology and neuroscience - Nieman Journalism Lab at Harvard

The Acetone Indigo Red Dehydrating Agent IF203 Induces HepG2 Cell Deat | OTT – Dove Medical Press

Yinghui Shang, 1 Qinghai Wang, 2 Jian Li, 1 Qiangqiang Zhao, 1 Xueyuan Huang, 1 Hang Dong, 1 Haiting Liu, 1 Ye Zhang, 3 Junhua Zhang, 1 Rong Gui, 1 Xinmin Nie 4

1Department of Blood Transfusion, The Third Xiangya Hospital, Central South University, Changsha, Peoples Republic of China; 2Department of Cardiology, The Second Hospital of Shandong University, Jinan, Peoples Republic of China; 3Department of Cell Biology, School of Basic Medicine, Peking University, Beijing, Peoples Republic of China; 4Clinical Laboratory of the Third Xiangya Hospital, Central South University, Changsha, Peoples Republic of China

Correspondence: Rong GuiDepartment of Blood Transfusion, The Third Xiangya Hospital, Central South University, No. 138 TongziPo Street, Changsha, Hunan 410013, Peoples Republic of ChinaTel/Fax +86-731-8861 8513Email aguirong@163.comXinmin NieClinical Laboratory of the Third Xiangya Hospital, Central South University, Changsha, No. 138 TongziPo Street, Changsha, Hunan 410013, Peoples Republic of ChinaTel/Fax +86-731-8861 8577Email niexinmin7440@sina.com

Background: Isatin derivatives have extensive biological activities, such as antitumor. IF203, a novel isatin derivative, has not previously been reported to have antitumor activity.Methods: Acid phosphatase assays (APAs) and Ki-67 immunohistochemistry were used to detect the proliferation of HepG2 cells. Transmission electron microscope (TEM) was applied to detect ultrastructural changes. Flow cytometry (FCM) was used to detect cell cycle, apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) of HepG2 cells in vitro. TUNEL, MMP and ROS immunofluorescence assays were applied to assess apoptosis, MMP, and ROS of HepG2 cells in vivo. Western Blotting was applied to assess the levels of apoptosis- and autophagy-related proteins.Results: In this study, in vivo and in vitro experiments showed that IF203 possesses antitumor activity. The results of APAs and Ki-67 immunohistochemistry demonstrated that IF203 could inhibit the proliferation of HepG2 cells. Cell cycle assays, downregulation of Cyclin B1 and Cdc2, and upregulation of P53 suggested that IF203 could lead to G2/M cell cycle arrest. In addition, ultrastructural changes, apoptosis assays, TUNEL immunofluorescence results, upregulated expression of Bax, and downregulated expression of Bcl-2 suggest that IF203 can induce apoptosis in HepG2 cells. After IF203 treatment, intracellular ROS levels increased, MMP decreased, JC-1 green fluorescence was enhanced, and the levels of Caspase-9, Caspase-3 and Cytochrome C expression were upregulated, suggesting that IF203 could induce apoptosis of HepG2 cells through the mitochondrial apoptosis pathway. Moreover, characteristic apoptotic ultrastructural changes were accompanied by the appearance of many autophagy bubbles and upregulation of Atg5, Atg12, ULK1, Beclin-1 and LC3-II proteins, suggesting that IF203 could induce autophagy in HepG2 cells.Conclusion: This study showed that IF203 leads to the death of HepG2 cells through cell cycle arrest, apoptotic induction, and autophagy promotion.

Keywords: acetone indigo red dehydrating agent, IF203, cell cycle arrest, autophagy, apoptosis

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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The Acetone Indigo Red Dehydrating Agent IF203 Induces HepG2 Cell Deat | OTT - Dove Medical Press

Investigational drugs block bone loss in mice receiving chemotherapy – Mirage News

Bone loss that can lead to osteoporosis and fractures is a major problem for cancer patients who receive chemotherapy and radiation. Since the hormone estrogen plays an important role in maintaining bone health, bone loss is especially pronounced among postmenopausal women with breast cancer who are treated using therapies aimed at eliminating estrogen.

Men and children treated for other cancers also experience bone loss, suggesting that eliminating estrogen is not the only trigger leading to bone degeneration.

Studying mice, researchers from Washington University School of Medicine in St. Louis have found a driver of bone loss related to cancer treatment. They have shown that radiation and chemotherapy can halt cell division in bone, which results in a stress response referred to as senescence. According to the new study, cell senescence drives bone loss in female mice beyond that seen from the absence of estrogen alone. The researchers further found that this process occurs in males and females and is independent of cancer type. And perhaps most importantly, the researchers showed that such bone loss can be stopped by treating the mice with either of two investigational drugs already being evaluated in clinical trials.

The study appears Jan. 13 in Cancer Research, a journal of the American Association for Cancer Research.

Researchers have understood that this bone loss has to be due to more than just hormone loss, said senior author Sheila A. Stewart, professor of cell biology & physiology. Cancer patients who receive chemotherapy and radiation lose a lot more bone than women with breast cancer treated with aromatase inhibitors, which eliminate estrogen. And children who have not yet gone through puberty, and arent making much estrogen, also lose bone. We wanted to understand what causes bone loss beyond a lack of estrogen and whether we can do anything to stop it.

Stopping bone loss could improve quality of life for cancer patients. Bone loss leads to an increased risk of fractures that continues many years after treatment. This loss of bone density makes it much more likely that patients will develop fractures in the pelvis, hips and spine, which affect mobility and increase the risk of death.

The researchers studied bone loss in mice treated with two common chemotherapy drugs doxorubicin and paclitaxel as well as in mice that received radiation to one limb, to understand whether the bone loss effects were similar in different types of cancer therapies. In all situations, the treatments induced the process of cellular senescence.

Senescence is a chronic stress response in a cell that stops it from dividing and also results in the release of many molecules, some of which we showed drive bone loss, said Stewart, who is also the associate director for basic sciences at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine.

The cells in mouse bones that were most affected by the cancer therapies included those responsible for bone remodeling. These are sets of cells that strike a vital balance between dismantling old bone and building new bone in its place. This balance is disturbed in conditions such as osteoporosis, in which the bone-building cells can no longer keep up with the bone-dismantling cells. The new study suggests that the balance is even more off-kilter following cancer therapy: Bone-building cell activity slows down, and the activity of cells that remove old bone actually accelerates.

The researchers showed they could prevent bone loss in the mice if they took steps to remove the cells that are no longer dividing, thus eliminating the molecular signals that the cells produce that drive bone loss. Toward possible therapies, Stewart and her colleagues then showed they could achieve a similar effect with two different types of compounds that block these molecular signals.

The investigational drugs, a p38MAPK inhibitor and a MK2 inhibitor, block different parts of the same pathway leading to bone loss. Stewart and her colleagues also published a study in 2018 showing that the two inhibitors slowed the growth of metastatic breast cancer in mice. The p38MAPK inhibitor is being tested in U.S. clinical trials for inflammatory diseases, such as chronic obstructive pulmonary disease (COPD). And the MK2 inhibitor is about to be evaluated as a therapy for rheumatoid arthritis.

Cancer patients at risk of bone loss often are treated with drugs for osteoporosis, including bisphosphonates and denosumab. Both have some undesirable side effects, such as muscle and bone pain and, because of the way they work, they may be less desirable for children whose bones are still growing.

The inhibitors we studied have extremely low toxicity, so we are interested in exploring whether they could be an improved option to stop bone loss in children receiving cancer therapy, Stewart said. Were also interested in pursuing a clinical trial to evaluate these drugs in women with metastatic breast cancer to see if we can slow metastatic growth and also preserve bone health in these patients.

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Investigational drugs block bone loss in mice receiving chemotherapy - Mirage News

Clever Decoy That Neutralizes Viruses Points Way to Treat Viruses That Cross From Animals to Humans – SciTechDaily

The active part of Arenacept is shown as a rainbow-colored ribbon bound to the receptor-binding domain of Macho virus (grey surface representation). Credit: Weizmann Institute of Science

A host of disease-causing viruses called arenaviruses lurk in animal populations in various parts of the world, sometimes crossing over into humans. When they do cross over, they can be lethal, and only very few treatments exist. Researchers led by scientists at the Weizmann Institute of Science have now devised a clever decoy for these viruses that may keep them from spreading in the body.

Two disease-causing arenaviruses, known as Junn and Machupo, circulate through rodent populations, mainly in South America, and they can infect humans when people come in contact with affected rodents. Similar to Ebola, these diseases can cause the body to bleed out, and the only treatments, to date, are risky and complex, as they are taken from the blood of survivors.

The present study, which was reported in the journal Nature Communications on January 3, 2020, arose from an earlier research question in the group of Dr. Ron Diskin of the Institutes Structural Biology Department: how are certain arenaviruses able to move from rodents or other animals into humans? Comparing these viruses with members of the arenavirus family that are not infectious to humans, the researchers noted that the non-infectious viruses did not completely fit a particular receptor a protein complex on the cell membrane that serves as a viral entry point into human cells. But curiously, those that do infect humans were also not a perfect fit. They were just good enough to get by.

This observation led to another insight: Maybe the rodent cell receptors, which were a much better fit to the entry proteins on the viruses, could be used to intercept the viruses and lure them away from the human cells. There had been earlier attempts to develop such decoys sticky molecules designed to attract virus proteins explains Diskin, but these were based on the structures of human receptors, so they were identical to the ones on the bodys cells and thus unable to compete effectively. In contrast, a molecule based on a rodent receptor, he and his team reasoned, could far outcompete the human ones for binding to the virus.

Dr. Hadas Cohen-Dvashi, in Diskins group, led the next stage of the research, in which she surgically removed the very tip of the rodent receptor to which the virus binds and engineered it onto part of an antibody. The newly resulting molecule was called Arenacept.

Then the group began testing this molecule at first against pseudoviruses, engineered virus-like complexes which carry the entry proteins but that are not dangerous. Already at this stage, and in collaboration with the group of Dr. Vered Paler-Karavani of Tel Aviv University, the researchers noted that Arenacept not only bound strongly to the viruses, it recruited parts of the immune system to mount an attack against the viral invasion.

The next stages of testing took place in labs in the University of Texas, Galveston, USA, and in the Pasteur Institute, Lyon, France, which are equipped to test pathogens at the highest safety levels (BSL-4). Here, Arenacept was pitted against human receptors in lab tests simulating attacks by two of the real pathogenic viruses the Junn and Machupo viruses.

The researchers found Arenacept to be highly effective at sticking strongly to the viruses before these viruses could bind to the human receptors, and as with the pseudoviruses, they noted the activation of the immune response.

Because Arenacept is based on the entry point shared by all viruses in a given family, rather than on individual characteristics of each virus (as is the case with vaccines or antibodies), it should be equally effective against all the viruses in this family that cross to humans from animals and for that utilize the same receptor. It might even be effective against viruses from the same family that have not yet been discovered or newly-emergent ones, says Diskin.

All signs suggest Arenacept is non-toxic, and that it is also heat-resistant and stable, meaning it could be delivered to the remote areas where these diseases are endemic, he says. And the idea of creating decoys from mammal receptors might be applied to all sorts of other diseases that cross to humans from animals. Yeda Research and Development, the technology transfer arm of the Weizmann Institute of Science, has received a patent for Arenacept and is working with Diskin to advance clinical research.

Reference: Rational design of universal immunotherapy for TfR1-tropic arenaviruses by Hadas Cohen-Dvashi, Ron Amon, Krystle N. Agans, Robert W. Cross, Aliza Borenstein-Katz, Mathieu Mateo, Sylvain Baize, Vered Padler-Karavani, Thomas W. Geisbert and Ron Diskin, 3 January 2020, Nature Communications.DOI: 10.1038/s41467-019-13924-6

Also participating in this research were Aliza Borenstein-Katz of the Weizmann Institute of Science; Ron Amon of Tel Aviv University; Krystle N. Agans, Robert W. Cross and Thomas W. Geisbert of the University of Texas; and Mathieu Mateo, Sylvain Baize of the Pasteur Institute.

Dr. Ron Diskins research is supported by theMoross Integrated Cancer Center; theDr. Barry Sherman Institute for Medicinal Chemistry; theJeanne and Joseph Nissim Center for Life Sciences Research; and the estate of Emile Mimran.

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Clever Decoy That Neutralizes Viruses Points Way to Treat Viruses That Cross From Animals to Humans - SciTechDaily

Douglas Hanahan Appointed Distinguished Scholar of the Ludwig Institute for Cancer Research – Newswise

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Newswise JANUARY 14, 2020, New York Ludwig Cancer Research is pleased to announce the appointment of Douglas Hanahan as a Distinguished Scholar at the Lausanne Branch of the Ludwig Institute for Cancer Research. A pioneering molecular biologist and renowned cancer researcher, Hanahan has made several seminal discoveries in cancer biology and immunology over the course of his career.

Everybody working in cancer research today knows of Dougs iconic work, since much of it has had a profound influence on the field, said Chi Van Dang, scientific director of the Ludwig Institute. He continues to do outstanding, multidisciplinary research, providing significant insights into mechanisms of cancer progression and the tumor microenvironment. Ludwig researchers will benefit enormously from the insights and mentorship of such an accomplished scientist. We couldnt be happier to have him on board.

While still a Harvard graduate student working at the Cold Spring Harbor Laboratory in New York in the 1970s, Hanahan developed new and more efficient methods for gene cloning and bacterial genetic engineering. After earning his PhD, Hanahan stayed on at Cold Spring Harbor and by the late 1980s had developed among the first mouse models engineered to develop cancers in specific organs. He went on to use these models to examine the stages by which precancerous cells progress to invasive malignancies, the role cancer genes play in this transformation and the immune systems response to cells bearing novel mutations associated with cancers.

In collaboration with the late Judah Folkman, Hanahan identified in these mouse models the angiogenic switcha defined step in which the new blood vessels absolutely required for solid tumor growth are induced in the early stages of tumorigenesis. He and Folkman subsequently explored the pharmacological inhibition of that step, work that ultimately contributed to the development of anti-angiogenic drugs for cancer therapy.

Hanahan is also noted for his co-authorship with Ludwig MIT Director Robert Weinberg of The Hallmarks of Cancer, a landmark perspective on cancer biology published in Cell in 2000, as well as an update the pair published in the journal in 2011. Their essay drew from all corners of the sprawling field of cancer biology to create a unifying conceptual framework for understanding tumor initiation and progression, identifying a handful of capabilities cells must acquire to become malignant. The papers, which remain among the most influential publications in modern cancer biology, have shaped efforts to develop new cancer therapies.

Hanahans lab today continues to unravel the stages and drivers of tumor progression and investigate pharmacologic strategies to disrupt each step of the process. It also explores how the tumor microenvironment contributes to drug resistance, with a focus on its role in thwarting immune clearancea phenomenon that is being investigated from multiple angles by researchers at Ludwig Lausanne.

Working with me over the past seven years, Doug played an important part in making the Swiss Cancer Center in the Lemanic region a reality, and he is more than familiar with our goals and plans at the Lausanne Ludwig Branch, said Ludwig Lausanne Director George Coukos. His experience and scientific creativity will be of immeasurable value to the researchers here and, I expect, across the Ludwig organization.

Hanahan, who earned his bachelors degree in physics from MIT and his PhD in biophysics from Harvard in 1983, has been widely recognized for his contributions to cancer biology. He received the Lifetime Achievement Award from the American Association for Cancer Research (AACR) in 2014 and is an elected member of the American Academy of Arts & Sciences, the U.S. National Academies of Science and of Medicine, the AACR Academy and the European Molecular Biology Organization.

In addition to his Ludwig Distinguished Scholar appointment, Hanahan is currently Professor and Director of the Swiss Institute for Experimental Cancer Research within the School of Life Sciences at EPFL, the Swiss Federal Institute of Technology Lausanne and Co-director of the new multi-institutional Swiss Cancer Center Leman.

About Ludwig Cancer Research

Ludwig Cancer Research is an international collaborative network of acclaimed scientists that has pioneered cancer research and landmark discovery for 48 years. Ludwig combines basic science with the ability to translate its discoveries and conduct clinical trials to accelerate the development of new cancer diagnostics and therapies. Since 1971, Ludwig has invested $2.7 billion in life-changing science through the not-for-profit Ludwig Institute for Cancer Research and the six U.S.-based Ludwig Centers. To learn more, visit http://www.ludwigcancerresearch.org.

For further information please contact Rachel Reinhardt, rreinhardt@lcr.org or +1-212-450-1582

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Douglas Hanahan Appointed Distinguished Scholar of the Ludwig Institute for Cancer Research - Newswise

Aloin Inhibits the Proliferation and Migration of Gastric Cancer Cells | DDDT – Dove Medical Press

Ziqian Wang, 1, 2 Tuo Tang, 1, 2 Shengnan Wang, 1, 2 Tianyu Cai, 1, 2 Hong Tao, 1, 2 Qing Zhang, 1, 2 Shimei Qi, 1, 2 Zhilin Qi 1, 2

1Department of Biochemistry and Molecular Biology, Wannan Medical College, Wuhu, Anhui 241002, Peoples Republic of China; 2Anhui Province Key Laboratory of Active Biological Macro-Molecules, Wannan Medical College, Wuhu, Anhui 241002, Peoples Republic of China

Correspondence: Zhilin QiDepartment of Biochemistry and Molecular Biology, Wannan Medical College, 22 Wenchang West Road, Wuhu, Anhui 241002, Peoples Republic of ChinaEmail 422627721@qq.com

Background: Aloin has been reported to have many pharmacological effects including anti-inflammatory, anti-oxidant and anti-tumour activities. However, the precise molecular mechanisms underlying the anti-tumour properties of aloin are yet to be elucidated.Methods: HGC-27 and BGC-823 gastric cancer cells were treated with aloin. EdU and colony formation assays were used to detect the proliferation ability of cells. The migration of cells was detected using wound healing and transwell assays. Western blotting was used to detect the levels of cyclinD1, cyclin E1, MMPs, N-cadherin, E-cadherin and NOX2. The phosphorylation of Akt, mTOR, P70S6K, S6, Src, stat3 and IB were also detected by Western blotting. Flow cytometry was used to detect the cell cycle distribution.The location of p65 in cells was determined by using a confocal microscopy assay. The total amounts of ROS present in cells were measured using an ROS assay kit.Results: Here, we found that aloin inhibited the proliferation and migration of HGC-27 and BGC-823 gastric cancer cells using a combination of EdU, colony formation, wound healing and transwell assays. Further investigations revealed that aloin decreased the protein expression levels of cyclin D1, N-cadherin, and the matrix metalloproteinases (MMP)-2 and MMP-9; increased E-cadherin expression in a dose-dependent manner; inhibited reactive oxygen species (ROS) generation; and mediated the activation of Akt-mTOR, signal transducer and activator of transcription-3 (Stat3), and NF-B signalling pathways. Our results also indicated that aloin is able to attenuate the expression levels of the two regulatory proteins of nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2), p47phox and p22phox, but had no effect on the level of gp91phox. N-acetylcysteine treatment of gastric cancer cells inhibited ROS production and Akt-mTOR, Stat3, and IB phosphorylation. Taken together, our data suggest that aloin inhibits the proliferation and migration of gastric cancer cells by downregulating NOX2ROS-mediated activation of the Akt-mTOR, Stat3, and NF-B signalling pathways.Conclusion: Our findings suggest a potential role for aloin in the prevention of gastric cancer cell proliferation and migration and provide novel insights into the anti-cancer properties of aloin.

Keywords: aloin, gastric cancer, proliferation, migration, nicotinamide adenine dinucleotide phosphate oxidase 2, reactive oxygen species

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Aloin Inhibits the Proliferation and Migration of Gastric Cancer Cells | DDDT - Dove Medical Press

Antibiotics Could Be Promising Treatment for Form of Dementia – UKNow

LEXINGTON, Ky. (Jan. 10, 2020)Researchers at the University of Kentuckys College of Medicine have found that a class of antibiotics called aminoglycosides could be a promising treatment for frontotemporal dementia.

Results of their proof of concept study, which was a collaborative effort between UKs Department of Molecular and Cellular Biochemistry and the University of California San Franciscos Department of Pathology, were recently published in the journal,Human Molecular Genetics.

Frontotemporal dementia isthe most common type of early onset dementia. It typically begins between ages 40 and 65 and affects the frontal and temporal lobes of the brain, which leads to behavior changes, difficulty speaking and writing, andmemory deterioration.

A subgroup of patients with frontotemporal dementia have a specific genetic mutation that prevents brain cells from making a protein called progranulin. Although progranulin is not widely understood, its absence is linked to the disease.

A group led by Haining Zhu, a professor in UKs Department of Molecular and Cellular Biochemistry, discovered that after aminoglycoside antibiotics were added to neuronal cells with this mutation, the cells started making the full-length progranulin protein by skipping the mutation.

These patients brain cells have a mutation that prevents progranulin from being made. The team found that by adding a small antibiotic molecule to the cells, they could trick the cellular machinery into making it, said Matthew Gentry, a co-author of the study and the Antonio S. Turco Endowed Professor in the Department of Molecular and Cellular Biochemistry.

The researchers found two specific aminoglycoside antibiotics - Gentamicin and G418 - were both effective in fixing the mutation and making the functional progranulin protein. After adding Gentamicin or G418 molecules to the affected cells, the progranulin protein level was recovered up to about 50 to 60%.

These results could be promising to drug development. Currently, there are no effective therapies for any type of dementia.

After this preclinical proof of concept study, the next step is to study the antibiotics effects on mice with the mutation that causes frontotemporal dementia, Zhu says. Another focus is to possibly develop new compounds from Gentamicin and G418 that could be safer and more effective. Although Gentamicin is an FDA-approved medication, its clinical usage is limited as it is associated with a number of adverse side effects.

If we can get the right resources and physician to work with, we could potentially repurpose this drug. This is an early stage of the study, but it provides an important proof of concept that these aminoglycoside antibiotics or their derivatives can be a therapeutic avenue for frontotemporal dementia, said Zhu.

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Antibiotics Could Be Promising Treatment for Form of Dementia - UKNow

Phage therapy: A new old… – ScienceBlog.com

The fight against drug-resistant pathogens remains an intense one. While the Centers for Disease Controls (CDC) 2019 biggest threats report reveals an overall decrease in drug-resistant microbe-related deaths as compared to its previous report (2013) the agency also cautions that new forms of drug-resistant pathogens are still emerging.

Meanwhile, the options for treating infections by these germs are diminishing, confirming doctors and scientists worries about the end of the age of antibiotics.

We knew it was going to be a problem early on, said UC Santa Barbara chemistry and biochemistry professorIrene Chen. Basically as soon as penicillin was discovered, a few years later it was reported that there was a resistant organism. Thanks to factors such as horizontal gene transfer and rapid reproduction, organisms such as Gram-negative bacteria are able to evolve faster than we can produce antibiotics to control them.

So Chen and her research group are seeking alternatives to antibiotics, in a growing effort to head off the tide of incurable bacterial infections. In their work, the group has turned to bacteriophages, a naturally occurring group of viruses that colonize on bacteria.

Thats their natural function, really, to grow on and kill bacteria, said Chen, author of apaperthat appears in the Proceedings of the National Academy of Sciences. By taking advantage of the bacteriophages ability to home in on specific bacteria without damaging the rest of the microbiome, the researchers were able to use a combination of gold nanorods and near-infrared light to destroy even multidrug-resistant bacteria without antibiotics.

Phage therapy isnt new, Chen said. In fact, it has been used in the former Soviet Union and Europe for about a century, though they are seen largely as last-resort alternatives to antibiotics. Among the unresolved issues of phage therapy is the incomplete characterization of the phages biology a biology that could allow for unintended consequences due to the phages own rapid evolution and reproduction, as well as potential toxins the viruses may carry. Another issue is the all-or-nothing aspect of phage therapy, Chen added.

Its difficult to analyze the effect of a phage treatment, she said. You might see it completely work or you might see it completely fail, but you dont have the kind of dose response you want.

To surmount these challenges, the Chen lab developed a method of controlled phage therapy.

What we did was to conjugate the phages to gold nanorods, she explained. These phanorods were applied to bacteria on in-vitro cultures of mammalian cells and then exposed to near-infrared light.

Conjugated to phages,gold nanorods find their target: a bacterial cell wall

Photo Credit:COURTESY IMAGE

When these nanorods are photo-excited, they translate the energy from light to heat, Chen said, and that creates very high local temperatures.

The heat is enough to kill the bacteria, and it also kills the phages, preventing any unwanted further evolutions. The result is a guided missile of targeted phage therapy that also allows for dosage control. The lab found success in destroyingE. coli,P. aeruginosaandV. cholerae human pathogens that cause acute symptoms if left unchecked. They also were able to successfully destroyX. campestris, a bacteria that causes rot in plants.

In a collaboration with UC Santa Barbara mechanical engineerBeth Pruitt, the lab determined that while the heat successfully destroyed bacteria and phage, more than 80% of the mammalian cell culture underneath the bacteria biofilm survived.

Bacteria under fire: Green bacteria are alive, while the red ones are dead

Photo Credit:COURTESY IMAGE

This issue of whether it damages mammalian tissues is very important, Chen said. Work in nanotechnology and nanomedicine treating bacterial infections indicates that when its non-targeted, it really does burden the surrounding tissues.

The lab plans to investigate other possible phages to counter other bacteria, possibly engineering a photothermal method that could treat multiple bacterial infections.

Research on this study was conducted also by UCSB postdoctoral fellow Huan Peng (lead author), Raymond E. Borg and Liam P. Dow.

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Phage therapy: A new old... - ScienceBlog.com