Archive for category: E-News

E-News

Neurodermatitis genes influence other allergies

, /in /by

There’s a typical ‘career’ for some allergic people, and it starts very early on the skin: babies develop atopic dermatitis, food allergies may follow, then comes asthma and later on hay fever. A group of scientists led by Ingo Marenholz and Young-Ae Lee at the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), working with colleagues from several institutions, has now identified seven genetic risk loci for this course of disease. Two of these loci were previously unknown and mainly influence the connection between atopic dermatitis and asthma. According to the study, the regions that determine the risk for atopic dermatitis are mainly those that also determine the risk for the further development of the typical allergic career. This course of disease is also called the ‘atopic march.’ The scientists analysed data from nearly 20,000 people.
For their meta-analysis, the researchers concentrated on cases where atopic dermatitis preceded asthma. They included 12 studies with 2,428 patients and 17,034 healthy people. All of these studies were genome-wide association studies (GWAS) based on millions of genetic variants called Single Nucleotide Polymorphisms (SNPs).

It is the first GWAS for the atopic march and showed for the first time that there are specific genetic loci influencing the march’s unfortunate course. ‘Seen from a physician’s perspective, the prominent role of atopic dermatitis genes for later-onset of asthma is very interesting,“ says Young-Ae Lee. Max Delbrück Center for Molecular Medicine

Merck Millipore Accepts Silver Stevie® Award for AFS® E Water Purification Systems at the 2015 American Business AwardsSM

, /in /by

29 September 2015, Darmstadt, Germany — Merck Millipore, the Life Science division of Merck, accepted a Silver Stevie® Award for its AFS® E Water Purification Systems at a banquet held on Friday, September 11 in San Francisco. The award was conferred by The American Business AwardsSM, the premier business awards program in the United States.

The AFS® E systems won the silver award in the ‘Health & Pharmaceuticals – Products & Services’ category in an event dedicated to outstanding new products and technology industries. Finalists were announced in May from over 3,300 entries submitted, and Gold, Silver and Bronze winners were judged and determined by more than 200 U.S. executives. Created in 2002 to recognize the achievements of organizations and professionals worldwide, the Stevie® Awards are organized in six separate programs, including The American Business AwardsSM.

Merck Millipore was represented at the awards dinner by Mohamed Bacchus, Regional Director of Sales West – Lab Water, and Joseph Plurad, North America Field Marketing Manager – Lab Water. ‘These AFS® E water purification systems incorporate our latest innovative technologies,’ said Joseph. ‘I’m proud to accept this award on behalf of all my colleagues worldwide who helped develop and support these new systems. By listening attentively to our clinical laboratory users, we were able to take their demands — as well as unmet needs — into account. The result is impressive, with systems offering our clinical lab customers the best advanced water purification technologies, as well as a unique user interface, serviceability, and sustainability.’

The AFS® 40E, 80E, 120E and 150E Water Purification Systems provide an economical and reliable high-performance solution for clinical analyzers with daily pure water needs up to 3000 liters. These systems integrate Merck Millipore’s state-of-the-art Elix® electrodeionization module, unique E.R.A.™ technology that decreases costs by automatically optimizing water recovery based on feed water quality, as well as 24/7 real-time monitoring and remote control.
Details about The American Business AwardsSM and the list of finalists in all categories are available at: www.stevieawards.com/aba

For more information on www.merckmillipore.com/labwater

Additional Resources

> Download high resolution photo

If you would like to speak to a media relations expert, please contact: Alexandra Langlois + 33 (0)6 76 54 41 28 – alexandra.langlois@external.merckgroup.com

About Merck Millipore
Merck Millipore is the Life Science subsidiary of Merck, Darmstadt, Germany. As part of the global Life Science business of Merck, Merck Millipore offers a broad range of innovative performance products, services and business relationships that enable our customers’ success in research, development and production of biotech and pharmaceutical drug therapies. Through dedicated collaboration on new scientific and engineering insights, and as one of the top three R&D investors in the life science tools industry, the Life Science business of Merck serves as a strategic partner to customers and helps advance the promise of life science. Headquartered in Billerica, Massachusetts, the global business has around 10,000 employees, operations in 66 countries and 2014 revenues of €2.7 billion. Merck Millipore operates as EMD Millipore in the U.S. and Canada.
For more information, please visit www.merckmillipore.com

About Merck
Merck is a leading company for innovative and top-quality high-tech products in healthcare, life science and performance materials. The company has six businesses – Merck Serono, Consumer Health, Allergopharma, Biosimilars, Merck Millipore and Performance Materials – and generated sales of € 11.3 billion in 2014. Around 39,000 Merck employees work in 66 countries to improve the quality of life for patients, to foster the success of customers and to help meet global challenges. Merck is the world’s oldest pharmaceutical and chemical company – since 1668, the company has stood for innovation, business success and responsible entrepreneurship. Holding an approximately 70% interest, the founding family remains the majority owner of the company to this day. Merck, Darmstadt, Germany holds the global rights to the Merck name and brand. The only exceptions are Canada and the United States, where the company operates as EMD Serono, EMD Millipore and EMD Performance Materials.
For more information, please visit http://www.merckgroup.com/en/index.html

About the Stevie® Awards
Stevie® Awards are conferred in six programs: the Asia-Pacific Stevie® Awards, the German Stevie® Awards, The American Business AwardsSM, The International Business Awards, the Stevie® Awards for Women in Business, and the Stevie® Awards for Sales & Customer Service. Stevie® Award competitions receive more than 10,000 entries each year from organizations in more than 60 nations. Honoring organizations of all types and sizes and the people behind them, the Stevies™ recognize outstanding performances in the workplace worldwide. Learn more about the Stevie® Awards at http://www.StevieAwards.com

Merck Millipore, the M mark, AFS, and Elix are registered trademarks of, and E.R.A is a trademark of Merck KGaA, Darmstadt, Germany. Any other trademarks are the property of their respective owners.

Innovative Abbott tests help in detecting tuberculosis and drug resistance

, /in /by

According to the World Health Organization, in 2014, there was an estimated 9.6 million new cases of tuberculosis (TB). TB is one of the leading, potentially-fatal infectious diseases caused by a bacterium known as Mycobacterium tuberculosis (MTB) that commonly affects the lungs. In 2014, nearly 500,000 people developed resistance to the two most powerful, anti-TB drugs known as isoniazid (INH) and rifampicin (RIF).  These drug therapies have been used for decades to treat TB, but resistance is becoming widespread from inappropriate or incorrect use. Today, molecular tests from Abbott are available to help doctors diagnose tuberculosis and to detect resistance to INH and RIF. The first test, Abbott’s Realtime MTB (CE-marked), is designed to qualitatively detect MTB in samples from individuals suspected of having tuberculosis. The second test, the RealTime MTB RIF/INH Resistance, was recently CE-marked and is designed to identify single resistance to INH or RIF as well as resistance to both drugs. At this year’s 46th Union World Conference on Lung Health (Cape Town, South Africa), Abbott hosted a satellite symposium titled “Advancing to the Next Level of Molecular Testing for Mycobacterium Tuberculosis (MTB)”.

www.abbottmolecular.com

Genetics can increase the risk of heart disease in women

, /in /by

The researchers from University College London studied a group of genes that have previously been linked to an increased risk of disease in the arteries. They studied data from nearly 4,000 men and women from across Europe, comparing their genes, their artery thickness and their artery health.

The scientists, led by BHF Professor Steve Humphries, believe they have pinpointed the gene in the group that is associated with an increased risk of a heart attack or stroke in women, but not in men.

Called BCAR1, the gene they identified is involved in many processes in the body that are affected by the female sex hormone oestrogen. The researchers believe that a high risk version of the BCAR1 gene – the GG version – when combined with a woman’s naturally occurring high oestrogen levels, could lead to the increased risk of cardiovascular disease compared with the low risk version – the AA version. Men with the GG version of the BCAR1 gene do not seem to be affected.

Over the five-year study, women with the high risk BCAR1 gene – around a third of those studied – had an increased risk (6.1%) of having a heart attack, stroke or diseased blood vessels compared with those with the low risk version of the gene (2.5%).

Heart disease is the major cause of heart attack and someone has a heart attack in the UK every three minutes. Understanding what puts people at risk of heart attacks is an important part of finding ways to prevent them and potentially treat people with medication to lower their risk of having a heart attack. British Heart Foundation

Tumour suppressor genes curb growth in neighbouring cells

, /in /by

Researchers at IRB Barcelona unravel a role for tumour suppressor genes in restricting the growth of neighbouring cell populations.

The study might have implications for understanding the early events of tumorigenesis and the selection of the tumour-initiating cells.
The healthy development of an organism depends on its tissues and organs growing to the right size, stopping when they need to, and maintaining stability in their form and function. Correct development depends on the availability of nutrients to the cells in their environment, a process that is tightly controlled by signalling mechanisms that occur within and between the cells that form these structures. Disruptions in this signalling can lead to unbalanced growth within a tissue or organ, and can give rise to conditions such as cancer.

The TOR and PI3K signalling pathways regulate tissue growth according to nutrient availability, and are frequently over-activated in human cancer. In the study published, Institute for Research in Biomedicine (IRB Barcelona) PhD student Ana Ferreira and Group Leader and ICREA Research Professor Marco Milán report that the over-activation of these two pathways not only causes the excess growth of cells and tissues, but also restrict the growth of neighbouring cell populations.

They present evidence that the proteoglycan Dally, a protein that is known to modulate the spreading, stability and activity of the growth-promoting signalling molecule called Dpp (in flies) or TGF-β (in humans), is regulated by these two pathways and mediates the effects on neighbouring populations. “They do so by competing for Dpp”, says Ana Ferreira, first author of the paper and funded by a PhD fellowship from Portugal’s Fundação para a Ciência e a Tecnologia.

‘PTEN, a gene that negatively regulates the PI3K pathway, is one of the most commonly lost tumour suppressors in human cancer. Understanding whether this pathway also affects TGF-β spreading in mammals may help us to gain insight into the early events of tumorigenesis and the selection of the tumour-initiating cells,’ she confirms.

‘Tumour initiating cells might be selected by their ability to compete for limiting growth factors and their capacity to restrict the growth of neighbouring cell populations,’ says Marco Milán, head of the Development and Growth Control Laboratory at IRB Barcelona. ‘Seventy percent of men with prostate cancer are estimated to have lost a copy of the PTEN gene at the time of diagnosis. It will be interesting to determine whether this mechanism, identified in fruit flies, is also active in humans.’ IRB Barcelona

New cytoplasmic role for proteins linked to neurological diseases, cancers

, /in /by

Researchers at UT Southwestern Medical Center have identified a second role for a class of RNA-binding proteins, revealing new insights about neurological diseases and conditions associated with this protein such as autism, epilepsy, and certain types of cancer.

“These data should promote a re-evaluation of those diseases to see if this new function that we’ve identified contributes to those defects,” said senior study author Dr. Michael Buszczak, Associate Professor of Molecular Biology and with the Hamon Center for Regenerative Science and Medicine at UT Southwestern.

The study indicates that RNA-binding fox (Rbfox) proteins oversee translation of messenger RNA, or mRNA, into proteins. Using the fruit fly Drosophila as a model, researchers showed that the Rbfox1 protein, in particular, has this regulatory role.

Rbfox1 proteins were known to play a key role in splicing together coding portions of genes called exons to form mRNA, which is subsequently translated to form proteins. Splicing largely takes place within the nucleus of cells, where many Rbfox1 proteins are found. But there are also variants of Rbfox1 proteins found in the cytoplasm – the portion of the cell outside the nucleus – and the function of those cytoplasmic proteins had not been understood. 

“We found that cytoplasmic Rbfox1 represses the production of specific proteins,” Dr. Buszczak said.

The lead author of the study, UT Southwestern Molecular Biology graduate student Arnaldo Carreira-Rosario, found that Rbfox1 binds to specific elements at the ends of mRNA molecules, preventing these mRNAs from being translated into proteins. If Rbfox1 proteins are lost and mRNA is no longer repressed, that could lead to aberrant growth of cells, or cancers.

The researchers found that cytoplasmic forms of Rbfox1 were required for germ cell development in Drosophila. “Without this protein, the germ cells are blocked in a very specific stage of differentiation and just linger there. They can’t differentiate into mature eggs,” said Dr. Buszczak, an E.E. and Greer Garson Fogelson Scholar in Medical Research.

This block leads to sterility in female Drosophila and, in other contexts, can result in an inappropriate proliferation of cells, which underlies cancer.

Work by co-author Dr. Mani Ramaswami of Trinity College Dublin in Ireland points to a link between the newly identified function of Rbfox1 proteins and neuronal development and function, which could have important implications for a number of the neuronal disorders linked to disruption of Rbfox1.

“The idea is that loss of Rbfox1 causes disease by disrupting protein expression, not RNA splicing,” Dr. Buszczak said. “If this interpretation is correct, then it has implications for how one would develop therapeutics to treat the disease in question.” UT Southwestern Medical Center

New test may improve diagnosis and treatment of pancreatobiliary and other gastrointestinal cancers

, /in /by

By collecting samples from the portal vein — which carries blood from the gastrointestinal tract, including from the pancreas, to the liver — physicians can learn far more about a patient’s pancreatic cancer than by relying on peripheral blood from a more easily accessed vein in the arm.

Primary tumours shed cancerous cells, known as circulating tumour cells (CTCs), into the blood. These have been widely studied as prognostic biomarkers for various cancers. Because these cells are often larger, irregularly shaped and tend to cluster together, they get trapped in smaller vessels.

The authors hypothesized that most cells released from a gastrointestinal tumour would flow into the portal vein and then get sequestered by the narrow vessels in the liver. These cells would not reach the peripheral venous system. CTCs from gastrointestinal tumours are rarely identified in the peripheral blood until the cancer is widely metastatic.

To test this theory, researchers from the University of Chicago used an ultrasound-guided endoscope and a small needle to take blood from the portal vein during routine diagnostic endoscopies. They found CTCs in 100 percent of 18 patients with suspected tumours in the pancreas and bile ducts. Tests using peripheral blood samples, the standard method, detected tumours cells in only 4 of the 18 patients.

To test this theory, researchers from the University of Chicago used an ultrasound-guided endoscope and a small needle to take blood from the portal vein during routine diagnostic endoscopies. They found CTCs in 100 percent of 18 patients with suspected tumors in the pancreas and bile ducts. Tests using peripheral blood samples, the standard method, detected tumors cells in only 4 of the 18 patients.
‘We demonstrated that this method is potentially quite valuable as well as non-invasive, feasible and safe,’ said study director Irving Waxman, MD, professor of medicine and surgery and director of the Center for Endoscopic Research and Therapeutics at the University. ‘We had no complications related to portal vein blood acquisition.’ University of Chicago

Population-based screening study of asymptomatic persons to start in China using GastroPanel biomarkers to identify gastric cancer risk

, /in /by

A gastric cancer risk screening study will be organized in Chinese healthcare centres by the China Health Promotion Foundation. The foundation is a public organization, managed by the Chinese Ministry of Health.
The multi-centre study will be conducted by fifty to one hundred primary healthcare units. The screening of about half a million 40-80-year-old asymptomatic persons will be tested with GastroPanel biomarkers, delivered by Biohit Oyj. The parties have agreed not to disclose the value of the contract. Data collection and analysis, including evaluation, are planned to be finalized at the end of 2016. The sample collection has started in the summer of 2015.
GastroPanel is a non-invasive blood test for stomach health. The test diagnoses Helicobacter pylori infection and atrophic gastritis, caused by H. pylori infection or autoimmune disease. These results can be used to assess whether asymptomatic patients have an increased risk of gastric or esophageal cancer, peptic ulcer disease or risk of vitamin B12-, calcium-, magnesium- and iron malabsorption and if further examinations or treatments are needed.
According to CEO Liu Feng, Biohit Biotech (Hefei) Co., Ltd, ’The most important risk factors for stomach cancer are H. pylori infection and atrophic gastritis, which often are asymptomatic, and can be accurately detected by GastroPanel biomarkers used for this population-based screening. Early detection of risk groups is important for the effective prevention of gastric cancer.’
CEO Semi Korpela, Biohit Oyj said: ‘This is an outstanding opening for GastroPanel biomarkers in the screening of asymptomatic subjects to identify the risk groups for gastric cancer and vitamin B12 malabsorption among other things. Gastric cancer is the leading cause of cancer related mortality in China. The use of the very informative GastroPanel for the screening of gastric cancer risk offers the possibility of prevention and early detection of stomach cancers. Based on correct diagnosis, screening reduces sick leaves and loss of labour input, as well as self-medication with its associated risks. Early detection of risk conditions for gastric cancer and vitamin and mineral deficiencies saves healthcare costs and human suffering as well.’

www.biohithealthcare.cominvestor.relations@biohit.fi

Gene associated with a set of poorly understood rare diseases

, /in /by

IRB Barcelona has identified GEMC1 as a master gene for the generation of multiciliated cells—cells with fine filaments that move fluids and substances—which are found exclusively in the brain, respiratory tract, and reproductive system.

Defects in multiciliated cells lead to ciliopathies—rare and complex diseases that are poorly understood and for which not all causative genes have been identified.

The genomic sequencing of hundreds of patients with diverse types of ciliopathies has revealed that “in many cases the gene responsible is not known”, says Travis Stracker, head of the Genomic Instability and Cancer Lab at the IRB Barcelona. “So many people do not have a molecular diagnosis,” stresses the researcher. “Our work seeks to contribute to bridging this knowledge gap”.

A study on mice by Travis Stracker and his team, in collaboration with Vincenzo Costanzo’s laboratory at the FIRC Institute of Molecular Oncology (IFOM) in Milan, in which they reveal a gene candidate for a subtype of human ciliopathy. The gene in question, GEMC1, is indispensable for the generation of multiciliated cells specific to tissues such as the brain, trachea, lungs and oviducts.

The surface of multiciliated cells is covered by hundreds of cilia. These tiny, hairlike structures serve to circulate cerebrospinal fluid, remove mucus from the respiratory tract, and transport ovum through the oviduct, among other functions. Defects in the generation or function of these cells causes a subtype of ciliopathies called Mucociliary Clearance Disorders.

Specifically, GEMC1-deficient mice produced by Stracker reproduce the symptoms of a rare disease called RGMC (Reduced Generation of Multiple Motile Cilia)—a condition that causes hydrocephaly, severe respiratory infections, and infertility. The work, led by IRB Barcelona PhD student Berta Terré and IFOM postdoctoral researcher Gabriele Piergiovanni, reports that GEMC1 regulates the only two genes known to date that underlie this disease, Multicilin and Cyclin O, thus making it a potential candidate gene for RGMC.

In addition, the study has revealed that GEMC1 is one of the most important genes in the gene signalling cascade for the production of multiciliated cells. This means that this gene affects many others that depend on its expression. The gene expression analysis of this first study has revealed at least 10 new candidate genes related to cilia, as well as dozens that were already known or suspected of being involved in the function of cilia. IRB Barcelona

New way to find DNA damage

, /in /by

University of Utah chemists devised a new way to detect chemical damage to DNA that sometimes leads to genetic mutations responsible for many diseases, including various cancers and neurological disorders.

“We are one step closer to understanding the underlying chemistry that leads to genetic diseases,” says Cynthia Burrows, distinguished professor and chair of chemistry at the university. “We have a way of marking and copying DNA damage sites so that we can preserve the information of where and what the damage was.”

Jan Riedl, a University of Utah postdoctoral fellow and the study’s first author, says 99 percent of DNA lesions – damage to the chemical bases known as A, C, G and T that help form the DNA double helix – are repaired naturally. The rest can lead to genetic mutations, which are errors in the sequence of bases and can cause disease. The new method can “identify and detect the position of lesions that lead to diseases,” he says.

Burrows says: “We are trying to look for the chemical changes in the base that can lead the cell to make a mistake, a mutation. One of the powerful things about our method is we can read more than a single damaged site [and up to dozens] on the same strand of DNA.”

The chemists say their new method will let researchers study chemical details of DNA lesions or damage. Such lesions, if not repaired naturally, accumulate over time and can lead to mutations responsible for many age-related diseases, including colon, breast, liver, lung and melanoma skin cancers; clogged arteries; and neurological ailments such as Huntington’s disease and Lou Gehrig’s disease.

“A method capable of identifying the chemical identity and location in which lesions appear is crucial for determining the molecular etiology [cause] of these diseases,” Burrows and colleague write in their study.

The new method for finding DNA lesions combines other, existing techniques.

First, the researchers find the damage and cut it out of the DNA the same way a cell does naturally, using what is called “base excision repair,” the discovery of which won a Nobel Prize in Chemistry this year for Tomas Lindahl, a scientist in England.

Second, an “unnatural base pair” is inserted at the snipped-out DNA damage site to label it. Instead of natural base pairs C-G and A-T, the Utah chemists used a so-called third or unnatural base pair invented by chemists at the Scripps Research Institute in California. Burrows says her study demonstrates the first practical use of that invention.

Third, the DNA with the damage site labelled by an unnatural third base pair is then amplified or copied millions of times using a well-known existing method called PCR, or polymerase chain reaction. Burrows says the new study’s key innovation was to use base excision repair to snip out the damage and then to insert the unnatural base pair at the damage site, making it possible to make millions of copies of the DNA – a process that normally would be prevented by the damage.

Fourth, another chemical label, named 18-crown-6 ether, is affixed to the unnatural base pair on all the DNA strands, which are then read or sequenced using a kind of nanopore sequencing developed a few years ago by Burrows and Utah chemist Henry White. Such sequencing involves determining the order and location of bases on a DNA strand – including damage sites labell ed by unnatural bases – by passing the strand through a molecule-size pore or nanopore.

People are born with their genome or genetic blueprint of 3 billion base pairs, “and then stuff happens,” Burrows says. “There’s damage from oxidative stress due to inflammation and infection, too much metabolism, or environmental chemicals.”

The new method seeks “molecular details that define how our genome responds to what we eat and the air we breathe, and ends up being healthy or not,” she says. University of Utah

Latest issue of Clinical laboratory

March 2026

CLi Cover MRCH 2026
Digital edition
All articles Archived issues

Free subscription

View more product news

Get our e-alert

The leading international magazine for Clinical laboratory Equipment for everyone in the Vitro diagnostics

Sign up today
clinlab logo blackbg 1

Prins Hendrikstraat 1
5611HH Eindhoven
The Netherlands
info@clinlabint.com

PanGlobal Media is not responsible for any error or omission that might occur in the electronic display of product or company data.