Throughput: 480 tests/hour 580 tests/hour with ISE
Test items on board: 36 items + ISE 3 items
Reaction volume: 120– 300 micro-liter
Patient samples on board: 72 patient samples, 30 STAT samples
Reaction volume: 140– 300 micro-liter
Test items on board: 24 items + ISE 3 items / 36 items + ISE 3 items
Patient samples on board: 30 patient samples
Throughput: 270 tests/hour 450 tests/hour with ISE
R1: 140 ～ 300μl (1μl step）
R2: 20 ～ 260μl (1μl step）
News and Announcements
Familial Hypercholesterolemia (FH) is caused by a genetic defect that hinders the body"s ability to remove low-density lipoprotein (LDL) cholesterol from the blood. High LDL levels in the blood are more likely to result in narrowing of the arteries, which puts patients at substantially higher lifetime risk for heart disease and stroke at an early age.
The condition occurs in around 1 out of 220 people and it is estimated that there are 30 million people with FH worldwide. However, FH is significantly underdiagnosed, largely due to the wide spectrum of phenotypes caused by a range of pathogenic variants. It is reported that more than 90% of patients worldwide and more than one million in the USA remain undiagnosed. An expert panel led by the Geisinger Genomic Medicine Institute (Danville, PA, USA) has recommended that genetic testing should be the standard of care for patients who have a definite or probable diagnosis for FH based on clinical factors and family history. Wider use of genetic testing to identify FH patients is necessary, according to the expert panel, since cardiovascular conditions and other disease phenotypes might show up in a minority of patients, and there might be incomplete information on the prevalence of such conditions among relatives. Moreover, while patients with pathogenic FH variants generally have higher LDL-C levels, studies have shown a wide range of levels among patients.
The scientists recommended that those with very high LDL cholesterol and a positive family history of high cholesterol or early heart attack should be evaluated for pathogenic variants in at least three genes: low density lipoprotein receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9), though doctors may assess other genes based on a patient"s specific phenotype. More than 2,000 unique genetic variants associated with FH have been identified to date, with around half being classified as pathogenic or likely pathogenic. More than 90% of pathogenic variants are in LDLR, between 5% and 10% are in APOB, and less than 1% are in PCSK9. Genetic testing doesn"t always detect a pathogenic variant in one of these genes, and the authors noted that FH should be diagnosed clinically in the event of a negative test result.Geisinger Genomic Medicine Institute
Urinary tests have been studied for the detection of bladder tumors; however, most of these tests have not been implemented in clinical practice because of cost issues, practical aspects, or insufficient sensitivity or specificity as compared to the gold standard.
Bladder cancer, which ranks fifth among the most frequently diagnosed cancers in the EU, has a high disease recurrence rate, some 70%, requiring frequent follow-ups. The standard follow-up procedure includes a cystoscopy, and this procedure is coupled with a urine analysis to inspect for cancerous cells and, if needed, a biopsy of the suspect area. Scientists at the Radboud University Nijmegen Medical Center (Nijmegen, The Netherlands) and their European colleagues performed a single-arm, prospective, double-blind clinical study was in five leading urology centers in Europe on 440 patients who were recruited in their first year of follow-up. Results for cystoscopy and cytology were noted, and if a lesion was detected, the date and result of histological confirmation were recorded.
The team collected a urine sample for the Bladder EpiCheck test (Nucleix, Rehovot, Israel) – a urine test developed to monitor recurrence of bladder cancer according to 15 DNA methylation biomarkers. The test was performed on ≥10 ml of urine and processed within five days in a central laboratory. Processing includes centrifugation to separate the cell pellet, from which DNA is extracted. The extracted DNA is digested using a methylation-sensitive restriction enzyme that cleaves DNA at recognition sequences if it is unmethylated, while leaving methylated sequences intact. Digested DNA is then amplified via real-time polymerase chain reaction with locus-specific primers and probes (eight wells per sample), and the resulting data are analyzed using the Bladder EpiCheck software.Radboud University Nijmegen Medical Center
There is no accurate method for distinguishing between the hypervirulent strain from the classical strain of Klebsiella pneumoniae (cKp), which is most often seen in the Western hemisphere, and is less virulent and usually causes infections in hospital settings.
Several biomarkers have been discovered that can accurately identify hypervirulent K. pneumoniae (hvKp), a pathogen that infects completely healthy people and can cause blindness in one day and flesh-eating infections, brain abscesses and death in just a few days.
An international team of scientists led by those at the University at Buffalo (Buffalo, NY, USA) identified a biomarker to differentiate hvKp from cKp strains they chose to use clinical data to develop strain cohorts for evaluation, given that the inclusion of any bacterial genotypic or phenotypic information in the definition of strain cohorts could introduce bias. The hvKp-rich cohort consisted of 85 strains isolated from deidentified patients from Taiwan and the USA. Since most K. pneumoniae infections in the North America and the UK presumably are due to cKp strains, the 90 cKp-rich strain cohort was generated from randomly chosen, deidentified blood isolates from different countries.University at Buffalo
Elevated levels of prostate specific antigen (PSA) in the blood can be an indicator of prostate cancer and lead to further diagnostic investigations. Obese men have lower serum prostate-specific antigen (PSA) than comparably aged lean men, but the underlying mechanism remains unclear. A recent study determined the effect of obesity on PSA and the potential contributing mechanisms.
Scientists at the University of Adelaide (Adelaide, Australia) and their colleagues recruited a cohort of 1,195 men aged 35 years and over, with demographic, anthropometric (body mass index (BMI), waist circumference (WC) and serum hormone (serum testosterone (T), estradiol (E2), PSA and hematology assessments obtained over two waves was assessed. Men with a history of prostate cancer or missing PSA were excluded, leaving 970 men for the final analysis. Mixed-effects regressions and mediation analyses adjusting for hormonal and volumetric factors explore the potential mechanisms relating obesity to PSA.
The scientists reported that after adjusting for age, PSA levels were lower in men with greater WC. In a multivariable model including WC, age, E2/T and PlasV as predictors, no statistically significant associations were observed between with PSA and either WC or PlasV, while strong associations were observed with both E2/T and age. In the mediation analyses with PlasV as the mediator, the average causal mediation effect (ACME) explained roughly 0.2 of the total effect of WC on PSA, while when E2/T is a mediator; the ACME explained roughly 0.5 of the effect.University of Adelaide
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