Roche Accu-Chek® Inform II test strips chosen by CEGA Air Ambulance requirements for accuracy and ease-of-use
CEGA Air Ambulance has recently upgraded its blood glucose monitoring system to use the advanced Accu-Chek Inform II test strips from Roche. Ensuring accurate and reliable results across a wide range of glucose levels, these easy to use blood glucose test strips provide the performance criteria necessary for monitoring critically ill patients prior to, during and after emergency flight transfers.
“We require a reliable, easy to use, professional tool for blood glucose measurement,” comments CEGA Senior Flight Nurse, Stuart Cox. “After reviewing all the kits that are available on the market, we felt that the Roche Accu-Chek Inform II test strips best met our requirements for high quality patient care in the air ambulance environment. The user interface is very simple and straightforward to use anywhere and by any of our trained staff. In addition, the strips have a very good range compared to other systems, giving accurate results at both high and low glucose levels, which is essential for patient safety.”
Stress-induced insulin resistance and hyperglycaemia is common in critically ill patients [1,2,3] and so close monitoring of blood glucose levels is an important part of their care. Studies have shown that maintenance of appropriate glycaemic control in such patients improves morbidity and mortality [1,4,5].
“Providing international medical assistance, including the transportation of critical care patients around Europe, we use the Accu-Chek Inform II glucose strips to assess patients prior to the flight to make sure they are stable; during the transfer to monitor them and guide any necessary treatment; and then after the flight to assess their status before handing them over to the next medical team. The accuracy of the Accu-Chek Inform II strips ensures that patients get the right care at the right time, and we can have confidence in the results.”
The Accu-Chek Inform II test strips have undergone extensive evaluation, including studies at over 30 external sites as well as thorough internal testing [6]. The results of these evaluations demonstrate that the Accu‑Chek Inform II strips provide accurate and reliable blood glucose measurements under a variety conditions, including wide haematocrit and environmental ranges and in presence of maltose. Furthermore, the strips require a minimal sample volume of just 0.6µl and deliver accurate results from alternative sampling sites, such as the palm and forearm.
“The Accu-Chek Inform II strips mirror our needs for air ambulance work,” concludes Stuart. “They are well researched, with evidence-based performance. We also value the after sales and technical support we have received from Roche, which has been invaluable in the training of our staff.”
www.roche.co.ukwww.cega-air-ambulance.com.
1. Van den Berghe, G., Wouters, P., Weekers, F. et al (2001) N Engl. J. Med. 345: 1359-67 2. Van den Berghe, G. (2004) J. Clin. Invest. 114: 1187-1195 3. Mizock, B.A. Best Pract. Res. Clin. Endocrinol. Metab. 2001,15(4): 533 – 551. 4. Krinsley, J.S. (2004) Mayo Clin. Proc. 79:992-1000 5. Insulin in Intensive Care – The Leuven Protocol. Intensive Care Society website: http://www.ics.ac.uk/icmprof/pubsother.asp?menuid=86. Information available on request, Roche Diagnostics, Burgess Hill, UK.
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Researchers have identified a genetic signature for a severe, often painful food allergy – eosinophilic esophagitis – that could lead to improved diagnosis and treatment for children unable to eat a wide variety of foods.
The scientists, from Cincinnati Children’s Hospital Medical Center that they have pinpointed a dysregulated microRNA signature for eosinophilic esophagitis (EoE), a disease that also may cause weight loss, vomiting, heartburn and swallowing difficulties.
Interestingly, the dysregulated microRNA was reversible with steroid treatment, according to the study’s senior investigator, Marc E. Rothenberg, MD, PhD, director of Allergy and Immunology and the Center for Eosinophilic Disorders at Cincinnati Children’s. MicroRNAs are short segments of RNA that can regulate whether genetic messengers (mRNAs) are degraded or translated into protein.
‘The identification of biomarkers specific to EoE is a significant advancement for both the diagnosis and treatment of the disease,’ explains Rothenberg. ‘The microRNA signature provides an opportunity for more precise analysis of oesophageal biopsies.’
Rothenberg said children with EoE now undergo anaesthesia and invasive endoscopy to diagnose and monitor the allergy. The ability to determine the presence and status of EoE with a non-invasive method, such as blood test that measures microRNAs, would have a positive impact on individuals and families.
In the current study, investigators analyzed esophageal microRNA expression of patients with active EoE, steroid-induced EoE remission, patients with chronic (non-eosinophilic) esophagitis and of healthy individuals. Additionally, they assessed plasma microRNA expression of patients with active EoE, remission of EoE remission and of healthy individuals.
The researchers found that EoE was associated with 32 differentially regulated microRNAs and distinguishable from the non-eosinophilic forms of esophagitis (such as reflux disease). Esophageal eosinophil levels correlated significantly with expression of the most increased microRNAs, miR-21 and miR-223, and most decreased, miR-375. MiR-223 was also one of the most increased microRNAs in the plasma, along with miR-146a and miR-146b.
Notably, the expression of microRNAs dysregulated in patients with active EoE was normalised in patients with EoE who responded to steroid treatment. This suggests a significantly specific microRNA signature for disease activity points to its promise for use as a biomarker for EoE.
EurekAlert
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Charles Eberhart, M.D., Ph.D. Johns Hopkins scientists have published laboratory data refuting studies that suggest blood vessels that form within brain cancers are largely made up of cancer cells. The theory of cancer-based blood vessels calls into question the use and value of anticancer drugs that target these blood vessels, including bevacizumab (Avastin).
‘We don’t question whether brain cancer cells have the potential to express blood vessel markers and may occasionally find their way into blood vessels, but we do question the extent to which this happens,’ says Charles Eberhart, M.D., Ph.D., chief of neuropathology at the Johns Hopkins University School of Medicine. ‘In general, we find no evidence in our study that these vessels contain substantial amounts of cancer cells.’
Eberhart, professor of pathology, ophthalmology and oncology at Johns Hopkins, said he first encountered claims about the cancerous nature of tumour blood vessels about a year ago when he was invited to join students at a journal club meeting, a forum for discussing studies published in medical journals. ‘My first reaction to this research was ‘How could this be true?’’ says Eberhart. ‘Our clinical experience examining tissue from brain cancers does not support it.’
Studies have long demonstrated that malignant brain tumours contain large numbers of blood vessels to feed their growing demand for nutrients. The blood vessels are formed when tumours pump out growth factors that increase vessel production. Such studies opened the door to treatment strategies that specifically targeted blood-vessel growth and the vessel cells themselves.
More recently, scientists in Italy and the Memorial Sloan Kettering Cancer Center in New York published results of studies suggesting that these tumour blood vessels are made by primitive types of brain cancer cells that are a form of stem cells. In their studies, they found tumour markers on blood vessel cells in 20 to 90 percent of their brain cancer samples. The U.S./Italian research teams said their findings also suggested that the cancer-like blood vessels were more prone to drug resistance, potentially explaining why drugs like bevacizumab yield tumour-shrinking responses, but only for short periods. Bevacizumab is currently approved by the U.S. Food and Drug Administration for use in patients with colorectal, lung, kidney and brain cancers.
Eberhart said pathologists, including those who work on brain tissue, use certain tissue-based techniques to distinguish cancer cells from normal ones. When evaluating specimens of brain tissue removed during surgery for suspected cancer, he said, most pathologists agree that blood vessel cells in these specimens consistently lack the molecular changes associated with cancer cells, according to Eberhart. In fact, they often use these blood vessel cells as ‘normal controls’ to compare with potentially cancerous ones.
After the journal club experience, Eberhart teamed up with fellow neuropathologist Fausto Rodriguez, M.D., and colleagues at the Dana Farber Cancer Institute and Harvard Medical School in Boston to look more closely at the molecular features of blood vessel cells in brain cancer samples. They tested more than 100 samples from patients at Johns Hopkins and Dana Farber for EGFR and IDH1 markers, two common genes altered in brain cancer.
‘We also used a marker called CD34 to differentiate vascular [blood vessel] cells from other types of cells,’ says Rodriguez, assistant professor of pathology at Johns Hopkins. The research teams found no more than 10 percent of their samples contained vascular cells with EGFR or IDH1 cancer markers, and in those rare tumour samples, only a few cells exhibited those markers. The Johns Hopkins-Dana Farber-Harvard team tested all parts of the vessel walls for presence of the cancer markers.
Although the two groups used different markers to identify vessel cells, Rodriguez says ‘there is no marker that is absolute for each cell.’
Johns Hopkins Medical Institutions
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Researchers at Oregon State University have tapped into the extraordinary power of carbon ‘nanotubes’ to increase the speed of biological sensors, a technology that might one day allow a doctor to routinely perform lab tests in minutes, speeding diagnosis and treatment while reducing costs.
The new findings have almost tripled the speed of prototype nano-biosensors, and should find applications not only in medicine but in toxicology, environmental monitoring, new drug development and other fields.
More refinements are necessary before the systems are ready for commercial production, scientists say, but they hold great potential.
‘With these types of sensors, it should be possible to do many medical lab tests in minutes, allowing the doctor to make a diagnosis during a single office visit,’ said Ethan Minot, an OSU assistant professor of physics. ‘Many existing tests take days, cost quite a bit and require trained laboratory technicians.
‘This approach should accomplish the same thing with a hand-held sensor, and might cut the cost of an existing $50 lab test to about $1,’ he said.
The key to the new technology, the researchers say, is the unusual capability of carbon nanotubes. An outgrowth of nanotechnology, which deals with extraordinarily small particles near the molecular level, these nanotubes are long, hollow structures that have unique mechanical, optical and electronic properties, and are finding many applications.
In this case, carbon nanotubes can be used to detect a protein on the surface of a sensor. The nanotubes change their electrical resistance when a protein lands on them, and the extent of this change can be measured to determine the presence of a particular protein – such as serum and ductal protein biomarkers that may be indicators of breast cancer.
The newest advance was the creation of a way to keep proteins from sticking to other surfaces, like fluid sticking to the wall of a pipe. By finding a way to essentially ‘grease the pipe,’ OSU researchers were able to speed the sensing process by 2.5 times.
Further work is needed to improve the selective binding of proteins, the scientists said, before it is ready to develop into commercial biosensors.
‘Electronic detection of blood-borne biomarker proteins offers the exciting possibility of point-of-care medical diagnostics,’ the researchers wrote in their study. ‘Ideally such electronic biosensor devices would be low-cost and would quantify multiple biomarkers within a few minutes.’
Oregon State University
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A new JDRF-funded study shows that many of the genes known to play a role in type 1 diabetes (T1D) are expressed in pancreatic beta cells, suggesting that the cell responsible for producing insulin may be playing a part in its own destruction to lead to T1D. Researchers in Belgium suggest this interpretation after producing an extensive catalogue of more than 15,000 genes expressed in human islets, forming the most extensive characterisation of human islets reported to date.
The researchers, led by Decio Eizirik, M.D., Ph.D., professor and director of the Laboratory of Experimental Medicine at Universite Libre de Bruxelles in Brussels, Belgium, used a technique called RNA sequencing—a method that identifies all forms of transcribed RNAs in a cell—to assemble a catalogue that showed that more than 15,000 genes are expressed in healthy human islets. Transcribed RNA (ribonucleic acid) molecules serve as the vehicles through which a cell’s genetic information is expressed. The data has been made available to other researchers to be used for future studies of beta cell function.
In the study, the researchers found many of the previously known genes associated with T1D among the genes expressed in human islets. When the researchers exposed the human islets to agents (cytokines) released by immune cells that may trigger T1D, they noted changes in the expression patterns of these genes. This finding suggested that the islets may be contributing to the recruitment of immune cells as T1D starts to develop.
While conventional wisdom was that these genes played a role in T1D by affecting the function of the immune system, their expression in human islets led the scientists to consider the possibility that the beta cells—once seen as merely victims in T1D—might actually assist in their own attack by the immune system.
‘Based on our research, our understanding now is that type 1 diabetes in its early stages, is characterised by a dialog between beta cells and the immune system, instead of the previous view of beta cells as purely passive victims of the immune attack,’ said Dr. Eizirik. ‘We can now open our eyes a bit wider to the possible ways that type 1 diabetes can develop. As we expand our focus on beta cells, we could start to unearth more answers in the mystery of this disease.’
‘What we’re seeing is that beta cells may in fact be playing a larger role in triggering type 1 diabetes than we previously thought, and exploring this concept more deeply could lead to a better understanding of the what causes the autoimmune attack,’ said Julia Greenstein, Ph.D., JDRF’s assistant vice president for cure therapies. ‘Dr. Eizirik’s work is important to JDRF because it shows us that there is a need for more research on beta cell survival and health and its role as a potentially key part of the early disease process. Furthermore, the catalog of genes from this study will continue to support progress in many more areas of diabetes research.’
EurekAlert
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To solve a modern health crisis, Jon Graff, MD, PhD, is looking back millions of years. Dr. Graff, Professor of Developmental Biology, and his colleagues genetically alter fruit flies to have diabetes or obesity.
Jon Graff, MD, PhD: ‘We’re interested in unraveling the basis of metabolism,’ Dr. Graff said. ‘Our ability to control fat and glucose levels are basic, ancient functions. We try to explore the evolutionary underpinnings.’ At the center of Dr. Graff’s work is the concept of evolutionary conservation—the principle that once a gene appears in a species, it remains similar in other species that evolve from it. Ancestral mammals diverged from ancestral flies about 300 million years ago, but today, modern humans and modern flies share many genes.
Dr. Graff and his colleagues focus on the fruit fly Drosophila melanogaster, the roundworm C. elegans, and mice.
By inducing mutations and selecting for flies that have disorders in sugar metabolism—a condition he calls ‘flyabetes’—the researchers can identify genes that may prove relevant to human disease. Flies don’t have blood, having instead a blood-like substance called hemolymph, but fundamentally, their glucose regulation is comparable to a mammal’s.
In Drosophila and mice, the researchers found that a single gene called adipose regulates fat and insulin resistance. In mice, they found that fat stem cells reside in the blood vessel walls of fatty tissue, but not in vessels of other types of tissues.
‘If we understand how adipocytes (fat cells) form and how they function, we can hopefully find therapeutic targets to treat obesity-related diseases in humans,’ Dr. Graff said. For instance, if the triggers can be found that signal stem cells to become fat cells, it may be possible to turn off the process.
His research involves animal models, but Dr. Graff keeps humans and human health in mind. ‘We have our eyes on what could be of use clinically,’ he said.
He cofounded a company called Reata Pharmaceuticals that now has an experimental anti-inflammatory drug, bardoxolone methyl, in Phase III clinical trials. The trial is testing the efficacy and safety of bardoxolone methyl in people with chronic kidney disease and type 2 diabetes.
‘We’re trying to understand a public health problem of obesity and diabetes,’ he said. ‘The problem is well enumerated, and the vast majority of people understand that this is a burden physically, socially, and medically. It’s a huge cost for the country.’
T Southwestern Medical Center
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A team of researchers from the Hospital Universitario La Paz Research Institute (IdiPAZ, Madrid), LifeSequencing S.L. (Valencia), Era7 Bioinformatics (Madrid) and Roche Spain (Barcelona) announced on March 14th the sequencing of the whole genome of three antibiotic resistant strains of Klebsiella pneunomiae isolated from a recent outbreak in a Spanish hospital. The sequence data, generated using Roche’s 454 GS FLX+ System, is some of the first for this particular bacterial species, providing new insights into how antibiotic resistance evolves within this microorganism and can lead to hospital outbreaks.
Klebsiella pneumoniae is a bacterium frequently found in the mouth and gut of healthy humans. In most instances, it does not lead to disease but it can mutate opportunistically and cause diverse types of infections. The bacterium also has a significant capacity to acquire antibiotic resistance. Three closely related isolates of a pathogenic strain of K. pneumonia with increasing degrees of antibiotic resistance were obtained in the Microbiology department at Hospital Universitario La Paz and sequenced at LifeSequencing in Valencia, Spain using the long read GS FLX+ System, developed by 454 Life Sciences, a Roche Company. The sequencing data was assembled using the GS De Novo Assembler software and functional annotation was performed to identify the relevant genes codified in the three genomes with BG7, the optimized system developed by Era 7 Bioinformatics, providing rich functional annotation of 454 Sequencing data.
The researchers found that the three bacteria strains showed an increasing resistance pattern to a wide range of the antibiotics most commonly used at the hospital. Comparison of the genomes will give insights regarding how antibiotic resistance evolves within K. pneumonia and will aid in efforts to reduce the increasing prevalence of antibiotic resistance worldwide. In addition, the comparison of these genomes with other previously studied bacteria will help to understand how a microorganism that is part of our normal microbiome can become a dangerous pathogen.
“Fast and affordable sequencing of pathogenic bacteria is a huge qualitative and quantitative advance that is radically changing the way researchers and clinicians view the infectious disease process,” said Dr. Jesús Mingorance lead researcher at the Hospital Universitario La Paz. The GS FLX+ and GS Junior Systems from Roche are aiding in these pathogen detection and bacterial comparative genomics efforts worldwide. For life science research only. Not for use in diagnostic procedures.
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Women 65 or older who have even mild retinopathy, a disease of blood vessels in the retina, are more likely to have cognitive decline and related vascular changes in the brain, according to a multi-institutional study led by scientists at the University of California, San Francisco (UCSF).
The findings suggest that a relatively simple eye screening could serve as a marker for cognitive changes related to vascular disease, allowing for early diagnosis and treatment, potentially reducing the progression of cognitive impairment to dementia.
As retinopathy usually is caused by Type II diabetes or hypertension, a diagnosis could indicate early stages of these diseases, before they are clinically detectable. Early diagnosis could allow for lifestyle or drug interventions when they might be most effective.
‘Lots of people who are pre-diabetic or pre-hypertensive develop retinopathy,’ said the lead author of the study, Mary Haan, DrPH, MPH, UCSF professor of epidemiology and biostatistics. ‘Early intervention might reduce the progression to full onset diabetes or hypertension.’
The results were based on data from the Women’s Health Initiative Memory Study and the Site Examination study, two ancillary studies of the Women’s Health Initiative Clinical Trial of Hormone Therapy.
In the study, the team followed 511 women with an average starting age of 69, for 10 years. Each year, the women took a cognition test focused on short-term memory and thinking processes. In the fourth year, they received an exam to assess eye health. In the eighth year, they received a brain scan.
Of the full group of women, 39 women, or 7.6 percent, were diagnosed with retinopathy. On average, these women scored worse on the cognition test than the other women. They had more difficulty, for instance, recalling a list of several words five minutes after hearing them.
The women with retinopathy also had more damage to the blood vessels of the brain. They had 47 percent more ischemic lesions, or holes, in the vasculature overall and 68 percent more lesions in the parietal lobe. The lesions, associated with vascular disease and sometimes stroke, are believed to be caused by high blood pressure. They also had more thickening of the white matter tracks that transmit signals in the brain, which also appear to be caused by high blood pressure.
Notably, the women did not have more brain atrophy, which is associated with Alzheimer’s disease. This result indicates that retinopathy is a marker of neurovascular disease rather than Alzheimer’s disease, according to Haan.
University of California, San Francisco,
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The addition of changes in inflammatory biomarkers to established clinical variables improves the prediction of mortality in patients with chronic obstructive pulmonary disease (COPD), according to a new study.
‘COPD is characterised by low-grade inflammation, so we hypothesised that the addition of inflammatory biomarkers to established predictive factors would improve the prediction of mortality,’ said lead author Bartolome Celli, lecturer in medicine at Harvard Medical School and member of the Pulmonary and Critical Care Division of Brigham and Women’s Hospital in Boston. ‘We found that the addition of a panel of selected biomarkers to clinical variables significantly improved the ability of clinical variables to predict mortality in these patients.’
The researchers analysed prospectively collected data on 1,843 COPD patients from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) study. Of these 1,843 patients, 168 (9.1%) died during the three-year follow-up.
Clinical predictors of morality included age, BODE (Body-Mass Index, Airflow Obstruction, Dyspnea, and Exercise Capacity) index , and incidence of hospitalisations due to exacerbation’s of COPD in the year prior to the study. A predictive model for mortality using these clinical variables had a C-statistic (which measures the ability of how well a clinical prediction rule can correctly rank-order patients by risk) of 0.686. Adding interleukin-6 (IL-6) to the predictive model significantly improved the C-statistic to 0.708, and the addition of a panel of biomarkers including white blood cell counts, IL-6, C-reactive protein (CRP), interleukin-8 (IL-8), fibrinogen, chemokine (C-C-motif) ligand 18 (CCL-18), and surfactant protein D (SP-D) further improved the C-statistic to 0.726.
‘This panel of selected biomarkers was not only elevated in non-survivors in our cohort, but was associated with mortality over three years of follow-up after adjusting for clinical variables known to predict mortality in patients with COPD,’ said Dr. Celli. ‘Except for IL-6, these biomarkers improved the predictive value of our model only marginally when considered individually, but they improved the model significantly when analyzed as a group.’
The study had several limitations, including the lack of a study adjudication committee to specify causes of death, the exclusion of some biomarkers thought to be important in the pathobiology of COPD, and the lack of a validating cohort.
‘Adding white blood cell counts and measurement of changes in systemic levels of IL-6, CRP, IL-8, fibrinogen, CCL-18, and SP-D significantly improves the ability of clinical variables to predict mortality in patients with COPD,’ said Dr. Celli. ‘This is the first study to show that the addition of biomarker levels to clinical predictors in COPD patients adds relevant prognostic information.’
EurekAlert
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Widely used antibiotics may increase incidence and severity of allergic asthma in early life, according to a University of British Columbia study.
The study shows that certain antibiotics that affect intestinal bacteria also had a profound impact on allergic asthma.
‘It has long been suspected that kids exposed to more antibiotics – like those in developed countries – are more prone to allergic asthma,’ says the study’s author, UBC microbiologist Brett Finlay. ‘Our study is the first experimental proof that shows how.’
Finlay’s team at UBC’s Dept. of Microbiology and Immunology and Michael Smith Laboratories examined how two widely used antibiotics – streptomycin and vancomycin – affected the bacterial ‘ecosystem’ in the gut. They found that vancomycin profoundly alters the bacterial communities in the intestine and increases severity of asthma in mouse models.
The same antibiotics do not impact adult mice’s susceptibility to asthma, indicating that early life is a critical period of establishing a healthy immune system.
Allergic asthma affects more than 100 million people worldwide and its prevalence is increasing on average by 50 per cent every decade, particularly among children in industrialized countries. According to the Asthma Society of Canada, asthma affects at least 12 per cent of Canadian children.
The human gut is colonised by approximately 100 trillion bacteria, and contains upwards of 1,000 bacterial species. While not fully understood, these micro-organisms, known as ‘gut flora,’ perform a host of useful functions, says Finlay.
‘Modern societal practices, such as improved sanitation methods and widespread antibiotic use, are causing the disappearance of ancestral species of bacteria in our gut that may be critical to a healthy immune system,’ says Finlay.
‘Our study shows this is the case with certain antibiotics and allergic asthma, and the gut-lung connection is also consistent with observations that incidence of asthma has not increased significantly in developing countries where antibiotic use is less prevalent – and in turn, the gut flora is permitted to fully develop.’
University of British Columbia
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Advanced blood glucose monitoring system provides superior patient safety during emergency flight transfer
, /in E-News /by 3wmediaRoche Accu-Chek® Inform II test strips chosen by CEGA Air Ambulance requirements for accuracy and ease-of-use
CEGA Air Ambulance has recently upgraded its blood glucose monitoring system to use the advanced Accu-Chek Inform II test strips from Roche. Ensuring accurate and reliable results across a wide range of glucose levels, these easy to use blood glucose test strips provide the performance criteria necessary for monitoring critically ill patients prior to, during and after emergency flight transfers.
“We require a reliable, easy to use, professional tool for blood glucose measurement,” comments CEGA Senior Flight Nurse, Stuart Cox. “After reviewing all the kits that are available on the market, we felt that the Roche Accu-Chek Inform II test strips best met our requirements for high quality patient care in the air ambulance environment. The user interface is very simple and straightforward to use anywhere and by any of our trained staff. In addition, the strips have a very good range compared to other systems, giving accurate results at both high and low glucose levels, which is essential for patient safety.”
Stress-induced insulin resistance and hyperglycaemia is common in critically ill patients [1,2,3] and so close monitoring of blood glucose levels is an important part of their care. Studies have shown that maintenance of appropriate glycaemic control in such patients improves morbidity and mortality [1,4,5].
“Providing international medical assistance, including the transportation of critical care patients around Europe, we use the Accu-Chek Inform II glucose strips to assess patients prior to the flight to make sure they are stable; during the transfer to monitor them and guide any necessary treatment; and then after the flight to assess their status before handing them over to the next medical team. The accuracy of the Accu-Chek Inform II strips ensures that patients get the right care at the right time, and we can have confidence in the results.”
The Accu-Chek Inform II test strips have undergone extensive evaluation, including studies at over 30 external sites as well as thorough internal testing [6]. The results of these evaluations demonstrate that the Accu‑Chek Inform II strips provide accurate and reliable blood glucose measurements under a variety conditions, including wide haematocrit and environmental ranges and in presence of maltose. Furthermore, the strips require a minimal sample volume of just 0.6µl and deliver accurate results from alternative sampling sites, such as the palm and forearm.
“The Accu-Chek Inform II strips mirror our needs for air ambulance work,” concludes Stuart. “They are well researched, with evidence-based performance. We also value the after sales and technical support we have received from Roche, which has been invaluable in the training of our staff.” www.roche.co.ukwww.cega-air-ambulance.com.
1. Van den Berghe, G., Wouters, P., Weekers, F. et al (2001) N Engl. J. Med. 345: 1359-67
2. Van den Berghe, G. (2004) J. Clin. Invest. 114: 1187-1195
3. Mizock, B.A. Best Pract. Res. Clin. Endocrinol. Metab. 2001,15(4): 533 – 551.
4. Krinsley, J.S. (2004) Mayo Clin. Proc. 79:992-1000
5. Insulin in Intensive Care – The Leuven Protocol. Intensive Care Society website: http://www.ics.ac.uk/icmprof/pubsother.asp?menuid=86. Information available on request, Roche Diagnostics, Burgess Hill, UK.
Genetic marker for painful food allergy points to improved diagnosis, treatment
, /in E-News /by 3wmediaResearchers have identified a genetic signature for a severe, often painful food allergy – eosinophilic esophagitis – that could lead to improved diagnosis and treatment for children unable to eat a wide variety of foods.
The scientists, from Cincinnati Children’s Hospital Medical Center that they have pinpointed a dysregulated microRNA signature for eosinophilic esophagitis (EoE), a disease that also may cause weight loss, vomiting, heartburn and swallowing difficulties.
Interestingly, the dysregulated microRNA was reversible with steroid treatment, according to the study’s senior investigator, Marc E. Rothenberg, MD, PhD, director of Allergy and Immunology and the Center for Eosinophilic Disorders at Cincinnati Children’s. MicroRNAs are short segments of RNA that can regulate whether genetic messengers (mRNAs) are degraded or translated into protein.
‘The identification of biomarkers specific to EoE is a significant advancement for both the diagnosis and treatment of the disease,’ explains Rothenberg. ‘The microRNA signature provides an opportunity for more precise analysis of oesophageal biopsies.’
Rothenberg said children with EoE now undergo anaesthesia and invasive endoscopy to diagnose and monitor the allergy. The ability to determine the presence and status of EoE with a non-invasive method, such as blood test that measures microRNAs, would have a positive impact on individuals and families.
In the current study, investigators analyzed esophageal microRNA expression of patients with active EoE, steroid-induced EoE remission, patients with chronic (non-eosinophilic) esophagitis and of healthy individuals. Additionally, they assessed plasma microRNA expression of patients with active EoE, remission of EoE remission and of healthy individuals.
The researchers found that EoE was associated with 32 differentially regulated microRNAs and distinguishable from the non-eosinophilic forms of esophagitis (such as reflux disease). Esophageal eosinophil levels correlated significantly with expression of the most increased microRNAs, miR-21 and miR-223, and most decreased, miR-375. MiR-223 was also one of the most increased microRNAs in the plasma, along with miR-146a and miR-146b.
Notably, the expression of microRNAs dysregulated in patients with active EoE was normalised in patients with EoE who responded to steroid treatment. This suggests a significantly specific microRNA signature for disease activity points to its promise for use as a biomarker for EoE. EurekAlert
Study refutes research claims that call into question use of vessel-targeting, anticancer drugs
, /in E-News /by 3wmediaCharles Eberhart, M.D., Ph.D. Johns Hopkins scientists have published laboratory data refuting studies that suggest blood vessels that form within brain cancers are largely made up of cancer cells. The theory of cancer-based blood vessels calls into question the use and value of anticancer drugs that target these blood vessels, including bevacizumab (Avastin).
‘We don’t question whether brain cancer cells have the potential to express blood vessel markers and may occasionally find their way into blood vessels, but we do question the extent to which this happens,’ says Charles Eberhart, M.D., Ph.D., chief of neuropathology at the Johns Hopkins University School of Medicine. ‘In general, we find no evidence in our study that these vessels contain substantial amounts of cancer cells.’
Eberhart, professor of pathology, ophthalmology and oncology at Johns Hopkins, said he first encountered claims about the cancerous nature of tumour blood vessels about a year ago when he was invited to join students at a journal club meeting, a forum for discussing studies published in medical journals. ‘My first reaction to this research was ‘How could this be true?’’ says Eberhart. ‘Our clinical experience examining tissue from brain cancers does not support it.’
Studies have long demonstrated that malignant brain tumours contain large numbers of blood vessels to feed their growing demand for nutrients. The blood vessels are formed when tumours pump out growth factors that increase vessel production. Such studies opened the door to treatment strategies that specifically targeted blood-vessel growth and the vessel cells themselves.
More recently, scientists in Italy and the Memorial Sloan Kettering Cancer Center in New York published results of studies suggesting that these tumour blood vessels are made by primitive types of brain cancer cells that are a form of stem cells. In their studies, they found tumour markers on blood vessel cells in 20 to 90 percent of their brain cancer samples. The U.S./Italian research teams said their findings also suggested that the cancer-like blood vessels were more prone to drug resistance, potentially explaining why drugs like bevacizumab yield tumour-shrinking responses, but only for short periods. Bevacizumab is currently approved by the U.S. Food and Drug Administration for use in patients with colorectal, lung, kidney and brain cancers.
Eberhart said pathologists, including those who work on brain tissue, use certain tissue-based techniques to distinguish cancer cells from normal ones. When evaluating specimens of brain tissue removed during surgery for suspected cancer, he said, most pathologists agree that blood vessel cells in these specimens consistently lack the molecular changes associated with cancer cells, according to Eberhart. In fact, they often use these blood vessel cells as ‘normal controls’ to compare with potentially cancerous ones.
After the journal club experience, Eberhart teamed up with fellow neuropathologist Fausto Rodriguez, M.D., and colleagues at the Dana Farber Cancer Institute and Harvard Medical School in Boston to look more closely at the molecular features of blood vessel cells in brain cancer samples. They tested more than 100 samples from patients at Johns Hopkins and Dana Farber for EGFR and IDH1 markers, two common genes altered in brain cancer.
‘We also used a marker called CD34 to differentiate vascular [blood vessel] cells from other types of cells,’ says Rodriguez, assistant professor of pathology at Johns Hopkins. The research teams found no more than 10 percent of their samples contained vascular cells with EGFR or IDH1 cancer markers, and in those rare tumour samples, only a few cells exhibited those markers. The Johns Hopkins-Dana Farber-Harvard team tested all parts of the vessel walls for presence of the cancer markers.
Although the two groups used different markers to identify vessel cells, Rodriguez says ‘there is no marker that is absolute for each cell.’ Johns Hopkins Medical Institutions
Nanotube technology leading to fast, lower-cost medical diagnostics
, /in E-News /by 3wmediaResearchers at Oregon State University have tapped into the extraordinary power of carbon ‘nanotubes’ to increase the speed of biological sensors, a technology that might one day allow a doctor to routinely perform lab tests in minutes, speeding diagnosis and treatment while reducing costs.
The new findings have almost tripled the speed of prototype nano-biosensors, and should find applications not only in medicine but in toxicology, environmental monitoring, new drug development and other fields.
More refinements are necessary before the systems are ready for commercial production, scientists say, but they hold great potential.
‘With these types of sensors, it should be possible to do many medical lab tests in minutes, allowing the doctor to make a diagnosis during a single office visit,’ said Ethan Minot, an OSU assistant professor of physics. ‘Many existing tests take days, cost quite a bit and require trained laboratory technicians.
‘This approach should accomplish the same thing with a hand-held sensor, and might cut the cost of an existing $50 lab test to about $1,’ he said.
The key to the new technology, the researchers say, is the unusual capability of carbon nanotubes. An outgrowth of nanotechnology, which deals with extraordinarily small particles near the molecular level, these nanotubes are long, hollow structures that have unique mechanical, optical and electronic properties, and are finding many applications.
In this case, carbon nanotubes can be used to detect a protein on the surface of a sensor. The nanotubes change their electrical resistance when a protein lands on them, and the extent of this change can be measured to determine the presence of a particular protein – such as serum and ductal protein biomarkers that may be indicators of breast cancer.
The newest advance was the creation of a way to keep proteins from sticking to other surfaces, like fluid sticking to the wall of a pipe. By finding a way to essentially ‘grease the pipe,’ OSU researchers were able to speed the sensing process by 2.5 times.
Further work is needed to improve the selective binding of proteins, the scientists said, before it is ready to develop into commercial biosensors.
‘Electronic detection of blood-borne biomarker proteins offers the exciting possibility of point-of-care medical diagnostics,’ the researchers wrote in their study. ‘Ideally such electronic biosensor devices would be low-cost and would quantify multiple biomarkers within a few minutes.’ Oregon State University
JDRF-funded study shows roles of beta cells and the immune system in Type 1 diabetes
, /in E-News /by 3wmediaA new JDRF-funded study shows that many of the genes known to play a role in type 1 diabetes (T1D) are expressed in pancreatic beta cells, suggesting that the cell responsible for producing insulin may be playing a part in its own destruction to lead to T1D. Researchers in Belgium suggest this interpretation after producing an extensive catalogue of more than 15,000 genes expressed in human islets, forming the most extensive characterisation of human islets reported to date.
The researchers, led by Decio Eizirik, M.D., Ph.D., professor and director of the Laboratory of Experimental Medicine at Universite Libre de Bruxelles in Brussels, Belgium, used a technique called RNA sequencing—a method that identifies all forms of transcribed RNAs in a cell—to assemble a catalogue that showed that more than 15,000 genes are expressed in healthy human islets. Transcribed RNA (ribonucleic acid) molecules serve as the vehicles through which a cell’s genetic information is expressed. The data has been made available to other researchers to be used for future studies of beta cell function.
In the study, the researchers found many of the previously known genes associated with T1D among the genes expressed in human islets. When the researchers exposed the human islets to agents (cytokines) released by immune cells that may trigger T1D, they noted changes in the expression patterns of these genes. This finding suggested that the islets may be contributing to the recruitment of immune cells as T1D starts to develop.
While conventional wisdom was that these genes played a role in T1D by affecting the function of the immune system, their expression in human islets led the scientists to consider the possibility that the beta cells—once seen as merely victims in T1D—might actually assist in their own attack by the immune system.
‘Based on our research, our understanding now is that type 1 diabetes in its early stages, is characterised by a dialog between beta cells and the immune system, instead of the previous view of beta cells as purely passive victims of the immune attack,’ said Dr. Eizirik. ‘We can now open our eyes a bit wider to the possible ways that type 1 diabetes can develop. As we expand our focus on beta cells, we could start to unearth more answers in the mystery of this disease.’
‘What we’re seeing is that beta cells may in fact be playing a larger role in triggering type 1 diabetes than we previously thought, and exploring this concept more deeply could lead to a better understanding of the what causes the autoimmune attack,’ said Julia Greenstein, Ph.D., JDRF’s assistant vice president for cure therapies. ‘Dr. Eizirik’s work is important to JDRF because it shows us that there is a need for more research on beta cell survival and health and its role as a potentially key part of the early disease process. Furthermore, the catalog of genes from this study will continue to support progress in many more areas of diabetes research.’ EurekAlert
Diabetic fruit flies and lessons they teach us
, /in E-News /by 3wmediaTo solve a modern health crisis, Jon Graff, MD, PhD, is looking back millions of years. Dr. Graff, Professor of Developmental Biology, and his colleagues genetically alter fruit flies to have diabetes or obesity.
Jon Graff, MD, PhD: ‘We’re interested in unraveling the basis of metabolism,’ Dr. Graff said. ‘Our ability to control fat and glucose levels are basic, ancient functions. We try to explore the evolutionary underpinnings.’ At the center of Dr. Graff’s work is the concept of evolutionary conservation—the principle that once a gene appears in a species, it remains similar in other species that evolve from it. Ancestral mammals diverged from ancestral flies about 300 million years ago, but today, modern humans and modern flies share many genes.
Dr. Graff and his colleagues focus on the fruit fly Drosophila melanogaster, the roundworm C. elegans, and mice.
By inducing mutations and selecting for flies that have disorders in sugar metabolism—a condition he calls ‘flyabetes’—the researchers can identify genes that may prove relevant to human disease. Flies don’t have blood, having instead a blood-like substance called hemolymph, but fundamentally, their glucose regulation is comparable to a mammal’s.
In Drosophila and mice, the researchers found that a single gene called adipose regulates fat and insulin resistance. In mice, they found that fat stem cells reside in the blood vessel walls of fatty tissue, but not in vessels of other types of tissues.
‘If we understand how adipocytes (fat cells) form and how they function, we can hopefully find therapeutic targets to treat obesity-related diseases in humans,’ Dr. Graff said. For instance, if the triggers can be found that signal stem cells to become fat cells, it may be possible to turn off the process.
His research involves animal models, but Dr. Graff keeps humans and human health in mind. ‘We have our eyes on what could be of use clinically,’ he said.
He cofounded a company called Reata Pharmaceuticals that now has an experimental anti-inflammatory drug, bardoxolone methyl, in Phase III clinical trials. The trial is testing the efficacy and safety of bardoxolone methyl in people with chronic kidney disease and type 2 diabetes.
‘We’re trying to understand a public health problem of obesity and diabetes,’ he said. ‘The problem is well enumerated, and the vast majority of people understand that this is a burden physically, socially, and medically. It’s a huge cost for the country.’ T Southwestern Medical Center
Spanish research team announce the sequencing of antibiotic resistance bacteria in recent hospital outbreak
, /in E-News /by 3wmediaA team of researchers from the Hospital Universitario La Paz Research Institute (IdiPAZ, Madrid), LifeSequencing S.L. (Valencia), Era7 Bioinformatics (Madrid) and Roche Spain (Barcelona) announced on March 14th the sequencing of the whole genome of three antibiotic resistant strains of Klebsiella pneunomiae isolated from a recent outbreak in a Spanish hospital. The sequence data, generated using Roche’s 454 GS FLX+ System, is some of the first for this particular bacterial species, providing new insights into how antibiotic resistance evolves within this microorganism and can lead to hospital outbreaks.
Klebsiella pneumoniae is a bacterium frequently found in the mouth and gut of healthy humans. In most instances, it does not lead to disease but it can mutate opportunistically and cause diverse types of infections. The bacterium also has a significant capacity to acquire antibiotic resistance. Three closely related isolates of a pathogenic strain of K. pneumonia with increasing degrees of antibiotic resistance were obtained in the Microbiology department at Hospital Universitario La Paz and sequenced at LifeSequencing in Valencia, Spain using the long read GS FLX+ System, developed by 454 Life Sciences, a Roche Company. The sequencing data was assembled using the GS De Novo Assembler software and functional annotation was performed to identify the relevant genes codified in the three genomes with BG7, the optimized system developed by Era 7 Bioinformatics, providing rich functional annotation of 454 Sequencing data.
The researchers found that the three bacteria strains showed an increasing resistance pattern to a wide range of the antibiotics most commonly used at the hospital. Comparison of the genomes will give insights regarding how antibiotic resistance evolves within K. pneumonia and will aid in efforts to reduce the increasing prevalence of antibiotic resistance worldwide. In addition, the comparison of these genomes with other previously studied bacteria will help to understand how a microorganism that is part of our normal microbiome can become a dangerous pathogen.
“Fast and affordable sequencing of pathogenic bacteria is a huge qualitative and quantitative advance that is radically changing the way researchers and clinicians view the infectious disease process,” said Dr. Jesús Mingorance lead researcher at the Hospital Universitario La Paz. The GS FLX+ and GS Junior Systems from Roche are aiding in these pathogen detection and bacterial comparative genomics efforts worldwide.
www.roche.comwww.idipaz.eswww.era7bioinformatics.comwww.lifesequencing.comFor life science research only. Not for use in diagnostic procedures.
Blood vessel disease of retina may be marker of cognitive decline
, /in E-News /by 3wmediaWomen 65 or older who have even mild retinopathy, a disease of blood vessels in the retina, are more likely to have cognitive decline and related vascular changes in the brain, according to a multi-institutional study led by scientists at the University of California, San Francisco (UCSF).
The findings suggest that a relatively simple eye screening could serve as a marker for cognitive changes related to vascular disease, allowing for early diagnosis and treatment, potentially reducing the progression of cognitive impairment to dementia.
As retinopathy usually is caused by Type II diabetes or hypertension, a diagnosis could indicate early stages of these diseases, before they are clinically detectable. Early diagnosis could allow for lifestyle or drug interventions when they might be most effective.
‘Lots of people who are pre-diabetic or pre-hypertensive develop retinopathy,’ said the lead author of the study, Mary Haan, DrPH, MPH, UCSF professor of epidemiology and biostatistics. ‘Early intervention might reduce the progression to full onset diabetes or hypertension.’
The results were based on data from the Women’s Health Initiative Memory Study and the Site Examination study, two ancillary studies of the Women’s Health Initiative Clinical Trial of Hormone Therapy.
In the study, the team followed 511 women with an average starting age of 69, for 10 years. Each year, the women took a cognition test focused on short-term memory and thinking processes. In the fourth year, they received an exam to assess eye health. In the eighth year, they received a brain scan.
Of the full group of women, 39 women, or 7.6 percent, were diagnosed with retinopathy. On average, these women scored worse on the cognition test than the other women. They had more difficulty, for instance, recalling a list of several words five minutes after hearing them.
The women with retinopathy also had more damage to the blood vessels of the brain. They had 47 percent more ischemic lesions, or holes, in the vasculature overall and 68 percent more lesions in the parietal lobe. The lesions, associated with vascular disease and sometimes stroke, are believed to be caused by high blood pressure. They also had more thickening of the white matter tracks that transmit signals in the brain, which also appear to be caused by high blood pressure.
Notably, the women did not have more brain atrophy, which is associated with Alzheimer’s disease. This result indicates that retinopathy is a marker of neurovascular disease rather than Alzheimer’s disease, according to Haan. University of California, San Francisco,
Inflammatory biomarkers improve the clinical prediction of mortality in COPD
, /in E-News /by 3wmediaThe addition of changes in inflammatory biomarkers to established clinical variables improves the prediction of mortality in patients with chronic obstructive pulmonary disease (COPD), according to a new study.
‘COPD is characterised by low-grade inflammation, so we hypothesised that the addition of inflammatory biomarkers to established predictive factors would improve the prediction of mortality,’ said lead author Bartolome Celli, lecturer in medicine at Harvard Medical School and member of the Pulmonary and Critical Care Division of Brigham and Women’s Hospital in Boston. ‘We found that the addition of a panel of selected biomarkers to clinical variables significantly improved the ability of clinical variables to predict mortality in these patients.’
The researchers analysed prospectively collected data on 1,843 COPD patients from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) study. Of these 1,843 patients, 168 (9.1%) died during the three-year follow-up.
Clinical predictors of morality included age, BODE (Body-Mass Index, Airflow Obstruction, Dyspnea, and Exercise Capacity) index , and incidence of hospitalisations due to exacerbation’s of COPD in the year prior to the study. A predictive model for mortality using these clinical variables had a C-statistic (which measures the ability of how well a clinical prediction rule can correctly rank-order patients by risk) of 0.686. Adding interleukin-6 (IL-6) to the predictive model significantly improved the C-statistic to 0.708, and the addition of a panel of biomarkers including white blood cell counts, IL-6, C-reactive protein (CRP), interleukin-8 (IL-8), fibrinogen, chemokine (C-C-motif) ligand 18 (CCL-18), and surfactant protein D (SP-D) further improved the C-statistic to 0.726.
‘This panel of selected biomarkers was not only elevated in non-survivors in our cohort, but was associated with mortality over three years of follow-up after adjusting for clinical variables known to predict mortality in patients with COPD,’ said Dr. Celli. ‘Except for IL-6, these biomarkers improved the predictive value of our model only marginally when considered individually, but they improved the model significantly when analyzed as a group.’
The study had several limitations, including the lack of a study adjudication committee to specify causes of death, the exclusion of some biomarkers thought to be important in the pathobiology of COPD, and the lack of a validating cohort.
‘Adding white blood cell counts and measurement of changes in systemic levels of IL-6, CRP, IL-8, fibrinogen, CCL-18, and SP-D significantly improves the ability of clinical variables to predict mortality in patients with COPD,’ said Dr. Celli. ‘This is the first study to show that the addition of biomarker levels to clinical predictors in COPD patients adds relevant prognostic information.’ EurekAlert
Exposure to antibiotics linked to severity of allergic asthma
, /in E-News /by 3wmediaWidely used antibiotics may increase incidence and severity of allergic asthma in early life, according to a University of British Columbia study.
The study shows that certain antibiotics that affect intestinal bacteria also had a profound impact on allergic asthma.
‘It has long been suspected that kids exposed to more antibiotics – like those in developed countries – are more prone to allergic asthma,’ says the study’s author, UBC microbiologist Brett Finlay. ‘Our study is the first experimental proof that shows how.’
Finlay’s team at UBC’s Dept. of Microbiology and Immunology and Michael Smith Laboratories examined how two widely used antibiotics – streptomycin and vancomycin – affected the bacterial ‘ecosystem’ in the gut. They found that vancomycin profoundly alters the bacterial communities in the intestine and increases severity of asthma in mouse models.
The same antibiotics do not impact adult mice’s susceptibility to asthma, indicating that early life is a critical period of establishing a healthy immune system.
Allergic asthma affects more than 100 million people worldwide and its prevalence is increasing on average by 50 per cent every decade, particularly among children in industrialized countries. According to the Asthma Society of Canada, asthma affects at least 12 per cent of Canadian children.
The human gut is colonised by approximately 100 trillion bacteria, and contains upwards of 1,000 bacterial species. While not fully understood, these micro-organisms, known as ‘gut flora,’ perform a host of useful functions, says Finlay.
‘Modern societal practices, such as improved sanitation methods and widespread antibiotic use, are causing the disappearance of ancestral species of bacteria in our gut that may be critical to a healthy immune system,’ says Finlay.
‘Our study shows this is the case with certain antibiotics and allergic asthma, and the gut-lung connection is also consistent with observations that incidence of asthma has not increased significantly in developing countries where antibiotic use is less prevalent – and in turn, the gut flora is permitted to fully develop.’ University of British Columbia