Background: The coronavirus disease 2019 (COVID-19) has escalated to be a global threat to public health. Analysis of the use of radiology resources may render us insight regarding the public health behavior during pandemic. We measured the influence COVID-19 had on the use of radiology resources in terms of the number of examinations performed, and turnaround time for portable radiography. Methods: This study was conducted at a tertiary hospital located in area where the prevalence of COVID-19 infection was low (0.01%). We compared the number of radiology examinations 1) before pandemic (in 2019) vs. during peak of pandemic (January to March 2020), and 2) before pandemic vs. after the peak of pandemic (April to June 2020) via t-tests. We repeated similar analyses for subgroups as follows: gender, age, department (outpatient, inpatient, emergency, screening), body parts, and modality. We also performed a survey of radiologic technologists regarding the turnaround time and rate-limiting step of portable radiography for patients with and without suspicion or confirmation of COVID-19. Results: Although not statistically significant, the daily number of examinations during the peak of pandemic decreased by 9 percentage points (2,638 vs. 2,413; difference [95% CI], −225 [−489, 38]; P = 0.094). The percentage change was especially notable for children, emergency, and screening department (25, 19, and 44 percentage points, respectively). After the peak of the pandemic, the number of examinations increased back to near the prepandemic level (2,638 vs. 2,588; −50 [−317, 218]; P = 0.71). The turnaround time for portable radiography tended to be longer for patients with suspicion or confirmation of COVID-19, with donning personal protective equipment being the major rate-limiting step. Conclusion The number of examinations decreased during the pandemic, reflecting the tendency of the public to refrain from seeking medical care even in a community of low infection risk. Nevertheless, burden of healthcare providers may not have decreased as much, considering longer turnaround time required for COVID-19 related examinations.

BACKGROUND: Abnormalities of the left ventricular diastolic function can be classified by pulsed Doppler echocardiography, but sometimes it may be difficult to differentiate normal diastolic function from pseudonormalization. Heart failure caused by increased left ventricular filling pressure is rather associated with pseudonormalization or restrictive pattern than normal pattem or relaxation abnormality. We investigated the usefulness of color M-mode Doppler echocardiographic indexes in differentiating normal relaxation from pseudonormalization after acute myocardial infarction. METHOD: Echocardiographic examination including color M-mode Doppler was performed in 44 patients with acute myocardial infarction between 10 and 14 days after attack. 34 patients without in-hospital congestive heart failure(CHF) were assigned as group I, and 10 patients with in-hospital CHF as group II. Flow propagation slope(FPS), time difference(TD) between the occurrence of peak flow velocity in the apical region and at the mitral tip, and normalized time difference(nTD) by mitral and apical distance were measured with color M-mode Doppler echocardiography. RESULTS: FPS was lower in group II(group I, 42.0+/-20.6cm/sec vs group II, 27.8+/-8.0cm/ sec , p=0.065). Both groups had similar TD and nTD. FPS was compared in patients with E/ A ratio of mitral inflow greater than 1(22 patients of group I and 7 patients of group II). Patients with E/A) 1 in group II had significantly lower FPS(group I, 52.1+/-17.5cm/sec vs group II, 31.0+/-7.4cm/sec ; p(0.01). CONCLUSION: FPS was significantly decreased after acute myocardial infarction in patients with in-hospital CHF compared with patients without in-hospital CHF, even when E/A ratio of mitral inflow was greater than 1. Therefore, FPS was an useful index in differentiating normal relaxation from pseudonormalization.
Echocardiography ; Echocardiography, Doppler* ; Echocardiography, Doppler, Pulsed ; Estrogens, Conjugated (USP)* ; Heart ; Heart Failure* ; Humans ; Myocardial Infarction* ; Relaxation

Arginase inhibition exhibits beneficial effects in vascular endothelial and smooth muscle cells. In human aortic smooth muscle cells (hAoSMCs), native low-density lipoprotein (nLDL) induced the production of interleukin-8 (IL-8) that is involved in the pathogenesis of cardiovascular diseases. Therefore, we examined the effect of arginase inhibition on IL-8 production and the underlying mechanism. In hAoSMCs, reverse transcription–PCR, western blotting and immunocytochemistry with MitoTracker confirmed that arginase II was confined predominantly to mitochondria. The mitochondrial membrane potential (MMP) was assessed using tetramethylrhodamine ethyl ester. The MMP decreased upon nLDL stimulation but was restored upon arginase inhibition. MMP loss caused by nLDL was prevented by treatment with the intracellular Ca(2+) chelator BAPTA-AM. In mitochondrial Ca(2+) measurements using Rhod-2 AM, increased mitochondrial Ca(2+) levels by nLDL were inhibited upon preincubation with an arginase inhibitor. Among the polyamines, spermine, an arginase activity-dependent product, caused mitochondrial Ca(2+) movement. The nLDL-induced MMP change resulted in p38 mitogen-activated protein kinase (MAPK) phosphorylation and IL-8 production and was prevented by the arginase inhibitors BAPTA and ruthenium 360. In isolated AoSMCs from ApoE(−/−) mice fed a high-cholesterol diet, arginase activity, p38 MAPK phosphorylation, spermine and mitochondrial Ca(2+) levels and keratinocyte-derived chemokine (KC) production were increased compared with wild-type (WT) mice. However, in AoSMCs isolated from arginase II-null mice, increases in MMP and decreases in mitochondrial Ca(2+) levels were noted compared with WT and were associated with p38 MAPK activation and IL-8 production. These data suggest that arginase activity regulates the change in MMP through Ca(2+) uptake that is essential for p38 MAPK phosphorylation and IL-8 production.

Mitochondria continuously fuse and divide to maintain homeostasis. An impairment in the balance between the fusion and fission processes can trigger mitochondrial dysfunction. Accumulating evidence suggests that mitochondrial dysfunction is related to neurodegenerative diseases such as Parkinson's disease (PD), with excessive mitochondrial fission in dopaminergic neurons being one of the pathological mechanisms of PD. Here, we investigated the balance between mitochondrial fusion and fission in the substantia nigra of a non-human primate model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. We found that MPTP induced shorter and abnormally distributed mitochondria. This phenomenon was accompanied by the activation of dynamin-related protein 1 (Drp1), a mitochondrial fission protein, through increased phosphorylation at S616. Thereafter, we assessed for activation of the components of the cyclin-dependent kinase 5 (CDK5) and extracellular signal-regulated kinase (ERK) signaling cascades, which are known regulators of Drp1(S616) phosphorylation. MPTP induced an increase in p25 and p35, which are required for CDK5 activation. Together, these findings suggest that the phosphorylation of Drp1(S616) by CDK5 is involved in mitochondrial fission in the substantia nigra of a non-human primate model of MPTP-induced PD.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Cyclin-Dependent Kinase 5 ; Cyclin-Dependent Kinases ; Dopaminergic Neurons ; Homeostasis ; Mitochondria ; Mitochondrial Dynamics ; Neurodegenerative Diseases ; Parkinson Disease ; Phosphorylation ; Phosphotransferases ; Primates ; Substantia Nigra

The function of microglia/macrophages after ischemic stroke is poorly understood. This study examines the role of microglia/macrophages in the focal infarct area after transient middle cerebral artery occlusion (MCAO) in rhesus monkeys. We measured infarct volume and neurological function by magnetic resonance imaging (MRI) and non-human primate stroke scale (NHPSS), respectively, to assess temporal changes following MCAO. Activated phagocytic microglia/macrophages were examined by immunohistochemistry in post-mortem brains (n=6 MCAO, n=2 controls) at 3 and 24 hours (acute stage), 2 and 4 weeks (subacute stage), and 4, and 20 months (chronic stage) following MCAO. We found that the infarct volume progressively decreased between 1 and 4 weeks following MCAO, in parallel with the neurological recovery. Greater presence of cluster of differentiation 68 (CD68)-expressing microglia/macrophages was detected in the infarct lesion in the subacute and chronic stage, compared to the acute stage. Surprisingly, 98~99% of transforming growth factor beta (TGFβ) was found colocalized with CD68-expressing cells. CD68-expressing microglia/macrophages, rather than CD206⁺ cells, may exert anti-inflammatory effects by secreting TGFβ after the subacute stage of ischemic stroke. CD68⁺ microglia/macrophages can therefore be used as a potential therapeutic target.
Brain ; Haplorhini ; Immunohistochemistry ; Infarction, Middle Cerebral Artery ; Inflammation ; Macaca mulatta ; Magnetic Resonance Imaging ; Microglia ; Middle Cerebral Artery ; Primates ; Stroke ; Transforming Growth Factor beta

Differentiated thyroid cancer demonstrates a wide range of clinical presentations, from very indolent cases to those with an aggressive prognosis. Therefore, diagnosing and treating each cancer appropriately based on its risk status is important. The Korean Thyroid Association (KTA) has provided and amended the clinical guidelines for thyroid cancer management since 2007. The main changes in this revised 2024 guideline include 1) individualization of surgical extent according to pathological tests and clinical findings, 2) application of active surveillance in low-risk papillary thyroid microcarcinoma, 3) indications for minimally invasive surgery, 4) adoption of World Health Organization pathological diagnostic criteria and definition of terminology in Korean, 5) update on literature evidence of recurrence risk for initial risk stratification, 6) addition of the role of molecular testing, 7) addition of definition of initial risk stratification and targeting thyroid stimulating hormone (TSH) concentrations according to ongoing risk stratification (ORS), 8) addition of treatment of perioperative hypoparathyroidism, 9) update on systemic chemotherapy, and 10) addition of treatment for pediatric patients with thyroid cancer.