Quick Sequential Organ Failure Assessment (qSOFA) to predict clinical outcome in tsutsugamushi disease patients in emergency department

Objective@#Tsutsugamushi disease is a febrile illness caused by tick bites. Delay in making the diagnosis and treatment cause an increase of the frequency of complications and mortality. The aim of this study was to determine quick sequential organ failure assessment (qSOFA) to predict the clinical outcome of scrub typhus patients in emergency departments. @*Methods@#This was a retrospective, observational study of patients with tsutsugamushi disease and who presented to the emergency department of an urban hospital and a rural tertiary hospital between January 2013 and December 2018. The demographic and laboratory data was collected through a chart review. Statistical analysis was performed by dividing the patients into the general ward admission group (general ward) and the intensive care unit admission group (ICU). @*Results@#Age, Acute Physiology and Chronic Health Evaluation II (APACHE) II score and laboratory tests such as pH, leukocyte count, C-reactive protein, and procalcitonin also showed significant differences between the general ward and ICU groups on the univariable logistic regression analysis, but only the qSOFA score among the variables showed a significant difference on the multivariate logistic regression analysis (P=0.014). @*Conclusion@#The qSOFA score will be a prompt and useful tool for predicting the prognosis of patients with tsutsugamushi disease in the emergency department.

RNAi: A Recent Revolutionary Tool for Understanding of Basic Biology / 대한임상미생물학회지

RNA interference (RNAi) is a gene-silencing technology by which small double-stranded RNAs are used to target the degradation of RNA with complementary sequence. RNAi is found in a wide variety of organisms (Caenorhabditis elegans, insects, plants, microorganisms and animals). With RNAi, we have harnessed the gene function to be explored, revolutionized our ability to perform large-scale genetic screens, and even therapeutic potential.

Measurement of Thrombus Precursor Protein in the Diseases Associated with Thrombosis and Changes after Heparin Therapy / 대한임상병리학회지

BACKGROUND: The relationship between thrombosis and atherosclerosis has long been recognized. It is important to diagnose them earlier and utilize thrombolytic agents earlier in the clinical diseases associated with thrombosis and atherosclerosis. So we measured the thrombus precursor protein (TpP) in these diseases and intended to investigate the changes after heparin therapy. METHODS: TpP concentration was measured in 17 patients with acute myocardial infarction (AMI), 7 patients with unstable angina (UA), 2 patients with aortic dissection (AD), 10 patients with other chest pain, and 9 patients with cerebral infarction and 18 healthy controls. We divided AMI into two groups, early presenters (n=10) who presented to the emergency room (ER) within 6 hours and late presenters (n=7) who presented to the ER after 6 hours of the onset of chest pain. Among the patients, in 24 patients treated with unfractionated heparin, the level of TpP was measured from plasma at 8 hours after therapy. We used the microtiter plate ELISA procedure. RESULTS: TpP was significantly increased in AD (mean+/-SD; 51.21+/-8.08 microgram/mL), AMI (12.07+/-9.62 microgram/mL), early AMI (11.39+/-9.25 microgram/mL), late AMI (13.05+/-10.78 microgram/mL), cerebral infarction (7.34+/-4.67 microgram/mL), and UA (7.05+/-4.72 microgram/mL) compared with healthy controls (3.03+/-1.48 g/ mL). Abnormal concentrations of TpP were observed in 2 of 2 patients (100%) with AD, 12 of 17 patients (70.6%) with AMI, 8 of 10 patients (80.0%) with early AMI, 4 of 7 patients (57.1%) with late AMI, 5 of 9 patients (55.6%) with cerebral infarction, 3 of 7 patients (42.9%) with UA, and 2 of 10 patients (20.0%) with other chest pain. Among the 24 patients following heparin therapy, the level of TpP did not show significant decrease after heparin therapy in the group of UA and AMI with increased TpP above the upper limit of normal (n=14). CONCLUSTIONS: TpP appears to be a sensitive marker of the clinical diseases associated with thrombosis and atherosclerosis. But, TpP measurement does not allow for the accurate monitoring in the treatment with unfractionated heparin.