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Tuesday, September 19, 2017

Improving Diagnosis of Zika Virus Infection for Pregnant Women !

Mosquito-borne Zika virus (ZIKV) was the cause of the recent large outbreak of Zika disease in America. Despite fever, Zika is a mild disease, although epidemics in recent years have demonstrated an association with the appearance of severe congenital malformations (microcephaly). Owing to ZIKV serology cross-reactivity with other tropical flaviviruses, the final diagnosis relies on nucleic acid amplification. Pregnant women in endemic areas should be investigated to follow infection and sequelae.

Background

Zika virus (ZIKV) belongs to the Flavivirus genus and is related to other viruses that are also transmitted by the bite of mosquitoes, such as dengue virus (DENV), yellow fever virus (YFV) and West Nile virus (WNV). The Flaviviridae family comprises single-strand RNA, membrane-enveloped viruses that frequently use Aedes aegypti as a vector. Despite ZIKV being discovered over 60 years ago, only since 2014 (in the French Polynesia Islands) and 2015 (Brazil and America) has it been evident that the virus can cause large outbreaks and epidemics that lead to a global public health emergency.








High-Sensitivity Assays for Troponin in Patients with Cardiac Disease !

Troponin is a widely used biomarker in patients with cardiac disease. The use of troponin is well established in patients with suspected acute myocardial infarction (AMI), but troponin measurement is also used in other acute and nonacute settings. In patients with suspected AMI, early decision-making is crucial to allow rapid treatment and further diagnostic evaluation. Current guidelines recommend serial measurements of troponin with a cut-off concentration at the 99th percentile to triage patients in the emergency department.

Newer, high-sensitivity assays for troponin enable the detection of distinctly lower concentrations. Using these assays and very low cut-off concentrations, several rapid diagnostic strategies have been reported to improve diagnosis in acute cardiac care. Furthermore, noncoronary and non-acute applications of troponin assays — for example as a biomarker in patients with heart failure, pulmonary embolism, or stable coronary artery disease — are on the horizon and might improve individual risk stratification.

In this Review, we provide an overview on the development of high-sensitivity assays for troponin, and their application in patients with cardiac disease.


Pathophysiological background of troponin and troponin release
in different settings. A schematic overview of myocardial structure
related to troponin (inset), as well as the plasma troponin concentrations 
in different clinical settings (young and healthy, elderly or chronic diseases,
myocardial injury, and myocardial infarction).



Non-Invasive Alternative To Amniocentesis? Experimental Test May Let Screen For Genetic Defects 5 Weeks Into Pregnancy

An experimental test that relies on an old-fashioned screening exam — the pap smear — may someday allow doctors to easily detect birth defects sooner than ever.

On Tuesday, Wayne State University (WSU) researchers revealed the latest encouraging findings on their creation, called “Trophoblast Retrieval and Isolation from the Cervix,” or TRIC for short. Using a pap smear, they scraped trophoblasts — the cells that eventually help form a fetus’ placenta — from pregnant women’s cervixes and genetically sequenced the fetal DNA found inside with next generation technology. They then compared these samples to those obtained from the mother, placenta, and fetus via conventional means.

Not only were the TRIC samples mostly made out of fetal DNA, indicating the low risk of contamination, but they matched up perfectly with the other fetal samples, validating the test’s overall accuracy. Even more importantly, the samples were taken as early as 5 weeks into pregnancy, blowing past the limit of other, invasive screening tests, such as amniocentesis, which can only be given starting at the end of the first trimester, 14 to 16 weeks in.

Researchers have developed a test that may be able to screen for birth defects
as early as five weeks into pregnancy.


Pneumonitis: Symptoms, Causes, and Treatments.

Pneumonitis is a disorder where a person has an allergic reaction in their lungs caused by certain inhaled substances. The condition is also referred to as hypersensitivity pneumonitis.

The reaction they have to these substances can cause air sacs in one or both lungs to become inflamed. If untreated, the condition can cause long-term damage to the lungs. However, pneumonitis can be completely reversed if action is taken quickly. 

In this article, we take a look at the symptoms, causes, and treatments of pneumonitis. We also examine the differences between the condition and the more familiar pneumonia.


Symptoms of pneumonitis include shortness of breath, rattling sounds
in the lungs, and coughing.
Read more: Pneumonitis: Symptoms, Causes, and Treatments.



Serum Level Measurements Improve Disease Risk Prediction.

Results obtained by using a commercially available uromodulin ELISA kit to analyze serum samples from individuals at risk for heart and circulatory system diseases indicated that this kidney-specific protein is a biomarker not only for kidney disease but also for cardiovascular diseases.

The glycoprotein uromodulin, also known as Tamm-Horsfall protein (THP), is synthesized exclusively in the kidneys and subsequently secreted. Low uromodulin concentrations in serum are a sensitive indicator for a loss of kidney function and thus play a role in the diagnosis of various renal diseases (nephropathies). When renal function is impaired, the uromodulin concentration in the serum sinks rapidly. Therefore, renal functional disorders can be identified at a very early stage of kidney damage, even in cases with few symptoms.

Uromodulin -a biomarker not only for kidney disease but also for cardiovascular diseases.



Source: LabMedica

Saturday, August 26, 2017

The Theory of Disappearing Microbiota and the Epidemics of Chronic Diseases.

In the present era, medical scientists have been confounded by the increasing incidence of multiple diseases across the world, beginning first in developed countries, and gradually spreading to other areas as they develop. These include the rises in cases of obesity, asthma, hay fever, food allergies, inflammatory bowel disease, juvenile (type 1) diabetes and autism, among many others. Are these diseases, which affect different body systems, unrelated or can a unified theory explain the increased incidence of all of these?

I believe that the latter possibility is true, and that the central theory to explain why these diseases have arisen and by what mechanism is based on modern changes in early life events that are related to the human microbiome. According to this theory, the microbiome of humans and of other animals is not accidental, but has been selected over long time periods to optimize host reproductive success through interactions between the microbiota and host physiology. Early life is the crucial period during which the adult microbiome becomes established, and development of the host and of the microbiota occur together in a conjoined manner through a dynamic equilibrium that follows a well-choreographed path. In early life, the context is set for the important developmental decisions that are required for the immune system to distinguish between what is self and what is not self, for metabolic organs to partition how much energy to expend or to save, and for the brain to determine how to respond socially to a person who might be either a friend or a foe.




Figure 1: A model for the interaction of the inherited microbiota with
early life immunological development in past and present children.



Heterogeneity in Tuberculosis.

Infection with Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), results in a range of clinical presentations in humans. Most infections manifest as a clinically asymptomatic, contained state that is termed latent TB infection (LTBI); a smaller subset of infected individuals present with symptomatic, active TB. Within these two seemingly binary states, there is a spectrum of host outcomes that have varying symptoms, microbiologies, immune responses and pathologies. Recently, it has become apparent that there is diversity of infection even within a single individual. A good understanding of the heterogeneity that is intrinsic to TB — at both the population level and the individual level — is crucial to inform the development of intervention strategies that account for and target the unique, complex and independent nature of the local host–pathogen interactions that occur in this infection. In this Review, we draw on model systems and human data to discuss multiple facets of TB biology and their relationship to the overall heterogeneity observed in the human disease.



Figure 1: A classical tuberculosis granuloma. The hallmark tuberculosis
granuloma is a highly organized collection of immune cells that aggregate
around a central necrotic core.


Source: NATURE REVIEWS IMMUNOLOGY


Monday, August 7, 2017

Association Between Genetic Variation And Influenza Severity.

It is estimated that in the USA influenza -related deaths in recent years have ranged from 12,000 to 56,000. Factors like age, obesity, pregnancy and such chronic health conditions as asthma, chronic lung disease and heart disease are associated with an elevated risk of complications and death.

However, there are no proven genetic markers of influenza risk with an established mechanism of action. Interferon Induced Transmembrane Protein 3 (IFITM3) is an anti-viral protein that helps to block influenza infection of lung cells and to promote survival of the killer T cells that help clear the infection in the airways.

Image: A scanning electron micrograph of a CD8+ T cell engaging a virus.
(Photo courtesy of Dennis Kunkel).
A group of scientists collaborating with those at St. Jude Children's Research Hospital (Memphis, TN, USA) searched for other possible IFITM3 variants that correlated with gene expression, levels of the IFITM3 proteins and were common in influenza patients in the USA. The search led to an IFITM3 variant known as rs34481144. They checked 86 children and adults in Memphis with confirmed influenza infections and found two-thirds of patients with the most severe symptoms carried at least one copy of the newly identified high-risk IFITM3 variant. The high-risk variant was found in just 32% of patients with milder symptoms.

The team also found an association between the newly identified high-risk variant and severe and fatal influenza infections in 265 critically ill pediatric patients hospitalized in one of 31 intensive care units nationwide. The patients did not have health problems that put them at high risk for severe influenza. Of the 17 patients in this group who died from the infection, 14 carried at least one copy of the newly identified high-risk variant. Further study revealed how binding differed between the high-risk and protective variants. Those differences led to lower levels of the IFITM3 protein in individuals with two copies of the high-risk gene variant compared to other patients. The Memphis influenza patients also had fewer of the killer T cells in their upper airways. The study identifies a new regulator of IFITM3 expression that associates with CD8+ T cell levels in the airways and a spectrum of clinical outcomes.

Paul Thomas, PhD, an immunologist and corresponding author of the study, said, “A genetic marker of influenza risk could make a life-saving difference, particularly during severe influenza outbreaks, by helping prioritize high-risk patients for vaccination, drug therapy and other interventions. These results raise hopes that this newly identified IFITM3 variant might provide such a marker.” The study was published on July 17, 2017, in the journal Nature Medicine.

Source: labmedica

Screen Your Blood Cholesterol Levels For Your Heart Disease Risk!

Researchers have developed a first-of-its-kind rapid assay for measuring effectiveness of a patient’s high-density lipoprotein cholesterol (HDL-C) in cleaning up arterial cholesterol. This HDL-C function test could improve risk assessment and diagnosis, and help provide and monitor more personalized treatments for cardiovascular disease (CVD) patients.

Image: Research suggests a HDL-C function test could improve risk assessment and diagnosis,
and help provide and monitor more personalized treatments for CVD patients
(Photo courtesy of iStock).
While scientists have yet to fully elucidate how HDL-C helps protects against heart disease, one of its chief functions is thought to be mediating the removal of cholesterol from blood vessel walls. Recent studies have indicated that the ability of a patient’s HDL-C to do this – known as its cholesterol efflux capacity (CEC) – is a better gauge of CVD development than HDL-C levels on their own. This means, for example, that a patient with low levels of HDL-C but optimal CEC could be protected against heart disease to a greater degree than a patient with high levels of HDL-C but low CEC. However, the current standard research procedures for measuring CEC involve radioisotope-labeled cholesterol and cultured macrophages, making these methods too complex and time-consuming for clinical testing.

In this study, a team of researchers led by Amane Harada, PhD, of Sysmex Corporation (Kobe, Japan) and Ryuji Toh, MD, PhD, of Kobe University Graduate School of Medicine (Kobe, Japan) has developed a test for HDL-C function that is simple enough for clinical use. With a turnaround time of less than 6 hours, the test determines cholesterol uptake capacity (CUC) – the ability of HDL-C to accept additional cholesterol – which the researchers found correlates with CEC but is easier to measure. 

They evaluated their CUC test in 156 patients who had undergone revascularization (such as a stent or bypass) due to coronary artery disease and who had subsequently decreased their low-density lipoprotein cholesterol to a healthier level of less than 100 mg/dL. The study found that low CUC in these patients after treatment was significantly associated with the recurrence of coronary lesions. The researchers also determined that combining CUC with established CVD risk factors significantly improved the power of established factors to forecast which patients would redevelop heart disease.

If further trials validate this test, it could enable healthcare providers to use CUC in conjunction with HDL-C levels to better predict who is at risk for CVD onset or recurrence. This test could also be used to develop new treatments that increase CEC and to monitor their efficacy in patients.

“A more efficient enhancement of the atheroprotective functions of HDL may decrease the risk of atherosclerosis and [cardiovascular disease], although it has been difficult to develop therapeutic drugs with the expected effects,” wrote Harada and Toh in this paper, “We consider that this can be explained in part by the lack of a convenient assay system to evaluate HDL functionality without complicated or time-consuming procedures. In this respect, our cholesterol uptake assay provides a concise, accurate, and robust system for high-throughput analysis at low cost.”

The study, by Harada A et al, was published in the May 2017 issue of the Journal of Applied Laboratory Medicine.

Source: labmedica

Cardiac Biomarkers and Clinical Decision Making

New video discusses the importance of cardiac biomarkers



In this video, hear from a former operating engineer at the White House who, despite an active lifestyle and basic good health, experienced sudden heart failure. In the context of his healthcare journey, the video highlights the role of cardiac biomarkers in clinical decision making and the diagnosis of a heart attack.

Diagnosed with advanced coronary artery disease, the patient underwent cardiac bypass surgery and was enrolled in a biomarker study during his postoperative course of treatment. “There’s no doubt that biomarkers have completely transformed how we care for our patients in cardiovascular medicine,” says the patient’s cardiologist.
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