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Abstract Objective Previous studies have revealed associations between hyperuricemia and microvascular diseases, but the association between hyperuricemia and abdominal aortic aneurysm (AAA) remains unclear. The aim of this study was to elucidate the pathogenesis and prove the relationship between AAA and hyperuricemia. Methods A retrospective study was performed to validate the growth rates of AAA in humans with different serum uric acid levels. A murine model of angiotensin II-induced AAA was used to assess the effects of hyperuricemia on AAA growth in vivo, and human aortic smooth muscle cells (HASMCs) were used to study the pathways involved in these effects in vitro. Results We analyzed data from 107 AAA patients and found that patients with serum uric acid levels above 9 mg/dl had higher AAA growth rates than patients with serum uric acid levels between 4 and 7.9 mg/dl. In vivo, induction of hyperuricemia increased the incidence of AAA formation and the abdominal aortic diameter in mice. The hyperuricemic mice exhibited higher levels of urate transporter 1 (URAT1) expression, phospho-extracellular signal-regulated kinase (p-ERK)1/2 expression, reactive oxygen species (ROS) levels and matrix metalloproteinase (MMP)-9 expression in the abdominal aorta than the control mice. Soluble uric acid increased the expression of URAT1, p-ERK1/2, and MMP-9 and the levels of ROS in HASMCs in vitro. Conclusions We have provided human evidence that hyperuricemia exacerbates AAA formation. In addition, our murine experimental evidence suggests that hyperuricemia exacerbates AAA formation and reveals that the URAT1/ERK1/2/ROS/MMP-9 pathway is among the pathways activated by uric acid in HASMCs.

Rupture of abdominal aortic aneurysms (AAAs) is one of the leading causes of sudden death in the elderly population. The osteogenic transcription factor runt-related gene (RUNX) encodes multifunctional mediators of intracellular signal transduction pathways in vascular remodeling and inflammation. We aimed to evaluate the roles of RUNX2 and its putative downstream target miR-424/322 in the modulation of several AAA progression-related key molecules, such as matrix metalloproteinases and vascular endothelial growth factor. In the GEO database, we found that male patients with AAAs had higher RUNX2 expression than did control patients. Several risk factors for aneurysm induced the overexpression of MMPs through RUNX2 transactivation, and this was dependent on Smad2/3 upregulation in human aortic smooth muscle cells. miR-424 was overexpressed through RUNX2 after angiotensin II (AngII) challenge. The administration of siRUNX2 and miR-424 mimics attenuated the activation of the Smad/RUNX2 axis and the overexpression of several AAA progression-related molecules in vitro. Compared to their littermates, miR-322 KO mice were susceptible to AngII-induced AAA, whereas the silencing of RUNX2 and the administration of exogenous miR-322 mimics ameliorated the AngII-induced AAA in ApoE KO mice. Overall, we established the roles of the Smad/RUNX2/miR-424/322 axis in AAA pathogenesis. We demonstrated the therapeutic potentials of miR-424/322 mimics and RUNX2 inhibitor for AAA progression.

Background: Beta-blockers are widely used for the treatment of arrhythmia, hypertension, and congestive heart failure. Major trauma causes significant blood loss and subsequent tachycardia and hypotension. Although beta-blockers may induce negative compensatory sympathetic responses to hemorrhagic shock, the effects of beta-blocker use before major trauma on posttrauma outcomes are controversial. Aim: We examined the association between the use of beta-blockers before major trauma and posttrauma outcomes using a nationwide population-based database. Methods: The data for this nationwide population-based retrospective cohort study were obtained from the National Health Insurance Research Database in Taiwan. A total of 2245 beta-blocker users were assigned to the study cohort, and another 8980 patients matched for age, sex, comorbidity, and medication use by inverse probability of treatment weighting formed the comparison cohort. The major outcome assessed was all-cause mortality during a 30-day follow-up period in major trauma patients with or without pretrauma beta-blocker use. Results: Our study included 2245 patients who used beta-blockers before major trauma. Individuals who used beta-blockers did not have a significantly higher cumulative risk of mortality than individuals who did not use beta-blockers (beta-blockers users: 17.19%, nonbeta-blockers users: 16.70%, P = 0.662). Conclusion: Pretrauma beta-blocker users did not have a higher mortality rate after a major trauma even after adjusting for several comorbidities and medications in a nationwide population database.

SARS-CoV-2 has spread rapidly, causing deaths worldwide. In this study, we evaluated the performance of the BD MAX Open System module for identifying viral pathogens, including SARS-CoV-2, in nasopharyngeal specimens from individuals with symptoms of upper respiratory tract infection. We developed and validated a rapid total nucleic acid extraction method based on real-time reverse transcription-polymerase chain reaction (RT-PCR) for the reliable, high-throughput simultaneous detection of common cold viral pathogens using the BD MAX Platform. The system was evaluated using 205 nasopharyngeal swab clinical samples. For assessment of the limit of detection (LoD), we used SARS-CoV-2, influenza A/B, and respiratory syncytial virus (RSV) RNA standards. The BD MAX dual multiplex real-time RT-PCR panel demonstrated a sensitivity comparable to that of the World Health Organization-recommended SARS-CoV-2 assay with an LoD of 50 copies/PCR. The LoD of influenza A/B and RSV was 100–200 copies/PCR. The overall percent agreement between the BD MAX panel and laboratory-developed RT-PCR test on 55 SARS-CoV-2-positive clinical samples was 100%. Among the 55 positive cases of COVID-19 analysed, no coinfection was detected. The BD MAX rapid multiplex PCR provides a highly sensitive, robust, and accurate assay for the rapid detection of SARS-CoV-2, influenza A/B, and RSV.

Heatstroke (HS) can cause acute lung injury (ALI). Heat stress induces inflammation and apoptosis via reactive oxygen species (ROS) and endogenous reactive aldehydes. Endothelial dysfunction also plays a crucial role in HS-induced ALI. Aldehyde dehydrogenase 2 (ALDH2) is a mitochondrial enzyme that detoxifies aldehydes such as 4-hydroxy-2-nonenal (4-HNE) protein adducts. A single point mutation in ALDH2 at E487K (ALDH2*2) intrinsically lowers the activity of ALDH2. Alda-1, an ALDH2 activator, attenuates the formation of 4-HNE protein adducts and ROS in several disease models. We hypothesized that ALDH2 can protect against heat stress-induced vascular inflammation and the accumulation of ROS and toxic aldehydes. Homozygous ALDH2*2 knock-in (KI) mice on a C57BL/6J background and C57BL/6J mice were used for the animal experiments. Human umbilical vein endothelial cells (HUVECs) were used for the in vitro experiment. The mice were directly subjected to whole-body heating (WBH, 42°C) for 1 h at 80% relative humidity. Alda-1 (16 mg/kg) was administered intraperitoneally prior to WBH. The severity of ALI was assessed by analyzing the protein levels and cell counts in the bronchoalveolar lavage fluid, the wet/dry ratio and histology. ALDH2*2 KI mice were susceptible to HS-induced ALI in vivo. Silencing ALDH2 induced 4-HNE and ROS accumulation in HUVECs subjected to heat stress. Alda-1 attenuated the heat stress-induced activation of inflammatory pathways, senescence and apoptosis in HUVECs. The lung homogenates of mice pretreated with Alda-1 exhibited significantly elevated ALDH2 activity and decreased ROS accumulation after WBH. Alda-1 significantly decreased the WBH-induced accumulation of 4-HNE and p65 and p38 activation. Here, we demonstrated the crucial roles of ALDH2 in protecting against heat stress-induced ROS production and vascular inflammation and preserving the viability of ECs. The activation of ALDH2 by Alda-1 attenuates WBH-induced ALI in vivo.

Acute renal infarction is an uncommon disease, which is frequently misdiagnosed or diagnosed late because of its nonspecific clinical presentation, and may result in irreversible damage to the renal parenchyma. Here, we present a case of acute renal infarction in a 51-year-old male, presenting with left flank pain and being diagnosed through computed tomography. We successfully performed catheter-directed thrombolysis to rescue the ischemic renal tissue and preserve the renal function.

Background: Taiwan is located in a subtropical area where there are approximately 50 kinds of land snakes and six principal kinds of venous snakes. Snakebite envenomation is not an uncommon issue in Taiwan. We design a study to obtain an understanding of the characteristics of snakebites and snakebite patients in a medical center in northern Taiwan. Materials and Methods: This was a retrospective medical records study of an 8-year period. We used the key word “snake” to search the emergency department (ED) diagnosis of all patients and then used antivenom management codes to select patients for inclusion. The species of snake involved, time and site of the bite, geographic data of the patients and patient outcomes were recorded. Results: In total, there were 125 snakebite patients (male 70%, female 30%). The snakes involved were Protobothrops mucrosquamatus (50%), followed by Trimeresurus stejnegeri (7%). The feet and ankles were the most frequently bitten areas (42.4%). The peak months were July and October. The average ED stasis time was 2 hours and 45 minutes, and 65.6% of snakebite patients received antivenom. In patients bitten by P. mucrosquamatus, there was a high surgical rate, 23.8% higher than those reported in other studies. No mortalities or side effects of antivenom were reported in these patients. Conclusion: We propose a clinical flow chart for physicians who are treating patients bitten by P. mucrosquamatus. Snakebites, especially those inflicted by P. mucrosquamatus, induce severe soft tissue swelling, which can mimic compartment syndrome. Antivenom for P. mucrosquamatus is the first and only choice of treatment. The amount of antivenom needs to match the clinical symptoms. Patients bitten by P. mucrosquamatus may need longer observation times than patients bitten by other species of snakes, in addition to toxicologist consultations, sonographic examinations, and measurement of the objective compartment pressure before surgery.

Background: Sleep disturbances and aversive cold stress (CS) are cardiovascular risk factors. This study investigates how homeostatic control autonomic baroreflex influences the hemodynamic perturbations evoked by paradoxical sleep deprivation (PSD) and CS.Methods: Conscious adult male rats were randomly divided into four groups (Sham/CON [control], Sham/PSD, sinoaortic denervation[SAD]/CON, and SAD/PSD). Spectral analysis and SAD were employed to evaluate the effects of a 72-hr PSD with 10-min CS onblood pressure variability and heart rate variability (BPV and HRV) at total power (TP) and three frequency power densities, very-low-frequency (VLF), low frequency (LF), and high frequency (HF). Results: Key findings showed: (I) Compared with the control shamsurgery (Sham/CON), in the natural baseline (PreCS) trial, SAD surgery (SAD/CON) causes high systolic blood pressure (SBP), heartrate (HR), increases LFBPV (low-frequency power of BPV), LF/HFHRV (the ratio LF/HF of HRV), and TPBPV (the total power ofBPV), but decreases HFHRV (high-frequency power of HRV) and VLFHRV (very-low-frequency power of HRV) than the Sham/CONdoes. In the CS trial, SAD/CON increases the CS-induced pressor, increases the CS-elicited spectral density, LF/HFHRV, but decreasesHFBPV than the Sham/CON does. (II) Compared with SAD/CON and Sham/PSD (PSD under sham surgery), in both PreCS and CStrials, SAD/PSD (PSD under SAD) causes high SBP and HR than both SAD/CON and Sham/PSD their SBP and HR. In PreCS, SAD-PSD also changes the spectral density, including increasing Sham-PSD’s LFBPV, LF/HFHRV, VLFBPV, and TPBPV but decreasingSham-PSD’s VLFHRV and TPHRV. However, in CS, SAD-PSD changes the CS-elicited spectral density, including increasing Sham-PSD’s VLFBPV, LF/HFHRV, and TPHRV but decreasing Sham-PSD’s HFBPV and LFBPV. Conclusion: The results suggest baroreflexcombined with other reflex pathways, such as inhibitory renorenal reflex, modulates the vascular and cardiorespiratory responses to PSDunder PreCS and subsequent CS trials.

The machine learning-assisted electrocardiogram (ECG) is increasingly recognized for its unprecedented capabilities in diagnosing and predicting cardiovascular diseases. Identifying the need for ECG examination early in emergency department (ED) triage is key to timely artificial intelligence-assisted analysis. We used machine learning to develop and validate a clinical decision support tool to predict ED triage patients’ need for ECG. Data from 301,658 ED visits from August 2017 to November 2020 in a tertiary hospital were divided into a development cohort, validation cohort, and two test cohorts that included admissions before and during the COVID-19 pandemic. Models were developed using logistic regression, decision tree, random forest, and XGBoost methods. Their areas under the receiver operating characteristic curves (AUCs), positive predictive values (PPVs), and negative predictive values (NPVs) were compared and validated. In the validation cohort, the AUCs were 0.887 for the XGBoost model, 0.885 for the logistic regression model, 0.878 for the random forest model, and 0.845 for the decision tree model. The XGBoost model was selected for subsequent application. In test cohort 1, the AUC was 0.891, with sensitivity of 0.812, specificity of 0.814, PPV of 0.708 and NPV of 0.886. In test cohort 2, the AUC was 0.885, with sensitivity of 0.816, specificity of 0.812, PPV of 0.659, and NPV of 0.908. In the cumulative incidence analysis, patients not receiving an ECG yet positively predicted by the model had significantly higher probability of receiving the examination within 48 h compared with those negatively predicted by the model. A machine learning model based on triage datasets was developed to predict ECG acquisition with high accuracy. The ECG recommendation can effectively predict whether patients presenting at ED triage will require an ECG, prompting subsequent analysis and decision-making in the ED.

Background: 2-Methoxyestradiol (2ME), a natural 17-β estradiol metabolite, is a potent anti-inflammatory agent, but its effect on ischemia/reperfusion (IR)-induced acute lung inflammation remains unknown. Annexin A1 (AnxA1), a glucocorticoid-regulated protein, is effective at inhibiting neutrophil transendothelial migration by binding the formyl peptide receptors (FPRs). We aimed to investigate whether 2ME upregulates the expression of AnxA1 and protects against IR-induced lung damage.Methods: IR-mediated acute lung inflammation was induced by ischemia for 40 min followed by reperfusion for 60 min in an isolated, perfused rat lung model. The rat lungs were randomly treated with vehicle or 2ME, and the functional relevance of AnxA1 was determined using an anti-AnxA1 antibody or BOC2 (a pan-receptor antagonist of the FPR). In vitro, human primary alveolar epithelial cells (HPAECs) and rat neutrophils were pretreated with 2ME and an AnxA1 siRNA or anti-AnxA1 antibody and subjected to hypoxia-reoxygenation (HR).Results: 2ME significantly decreased all lung edema parameters, neutrophil infiltration, oxidative stress, proinflammatory cytokine production, lung cell apoptosis, tight junction protein disruption, and lung tissue injury in the IR-induced acute lung inflammation model. 2ME also increased the expression of the AnxA1 mRNA and protein and suppressed the activation of nuclear factor-κB (NF-κB). In vitro, 2ME attenuated HR-triggered NF-κB activation and interleukin-8 production in HPAECs, decreased transendothelial migration, tumor necrosis factor-α production, and increased apoptosis in neutrophils exposed to HR. These protective effects of 2ME were significantly abrogated by BOC2, the anti-AnxA1 antibody, or AnxA1 siRNA.Conclusions: 2ME ameliorates IR-induced acute lung inflammation by increasing AnxA1 expression. Based on these results, 2ME may be a promising agent for attenuating IR-induced lung injury.

Coronavirus disease 2019 has become a worldwide pandemic. By April 7, 2020, approximately 1,279,722 confirmed cases were reported worldwide including those in Asia, European Region, African Region and Region of the Americas. Rapid and accurate detection of Severe Acute Respiratory Syndrome Virus 2 (SARS-CoV-2) is critical for patient care and implementing public health measures to control the spread of infection. In this study, we developed and validated a rapid total nucleic acid extraction method based on real‐time RT-PCR for reliable, high‐throughput identification of SARS-CoV-2 using the BD MAX platform. For clinical validation, 300 throat swab and 100 sputum clinical samples were examined by both the BD MAX platform and in-house real-time RT-PCR methods, which showed 100% concordant results. This BD MAX protocol is fully automated and the turnaround time from sample to results is approximately 2.5 h for 24 samples compared to 4.8 h by in-house real-time RT-PCR. Our developed BD MAX RT-PCR assay can accurately identify SARS-CoV-2 infection and shorten the turnaround time to increase the effectiveness of control and prevention measures for this emerging infectious disease.

Background/Aims: Hyperlipidemia induces dysfunction in the smooth muscle cells (SMCs) of the blood vessels, and the vascular remodeling that ensues is a key proatherogenic factor contributing to cardiovascular events. Chemokines and chemokine receptors play crucial roles in vascular remodeling. Here, we examined whether the hyperlipidemia-derived chemokine CCL5 and its receptor CCR5 influence vascular SMC proliferation, phenotypic switching, and explored the underlying mechanisms. Methods: Thoracoabdominal aorta were isolated from wild-type, CCL5 and CCR5 double-knockout mice (CCL5–/–CCR5–/–) fed a high-fat diet (HFD) for 12 weeks. Expression of the contractile, synthetic, and proliferation markers were assayed using immunohistochemical and western blotting. The effects of CCL5 and palmitic acid on cultured SMC proliferation and phenotypic modulation were evaluated using flow cytometry, bromodeoxyuridine (BrdU), and western blotting. Results: Wild-type mice fed an HFD showed markedly increased total cholesterol, triglyceride, and CCL5 serum levels, as well as significantly increased CCL5 and CCR5 expression in the thoracoabdominal aorta vs. normal-diet-fed controls. HFD-fed CCL5-/-CCR5-/- mice showed significantly decreased expression of the synthetic phenotype marker osteopontin and the proliferation marker proliferating cell nuclear antigen, and increased expression of the contractile phenotype marker smooth muscle α-actin in the thoracoabdominal aorta vs. wild-type HFD-fed mice. Human aorta-derived SMCs stimulated with palmitic acid showed significantly increased expression of CCL5, CCR5, and synthetic phenotype markers, as well as increased proliferation. CCL5-treated SMCs showed increased cell cycle regulatory protein expression, paralleling increased synthetic and decreased contractile phenotype marker expression. Inhibition of CCR5 activity by the specific antagonist maraviroc or its expression using small interfering RNA significantly inhibited human aortic SMC proliferation and synthetic phenotype formation. Therefore, CCL5 induces SMC proliferation and phenotypic switching from a contractile to synthetic phenotype via CCR5. CCL5-mediated SMC stimulation activated ERK1/2, Akt/p70S6K, p38 MAPK, and NF-κB signaling. NF-κB inhibition significantly reduced CCR5 expression along with CCR5-induced SMC proliferation and synthetic phenotype formation. Conclusions: Hyperlipidemia-induced CCL5/CCR5 axis activation serves as a pivotal mediator of vascular remodeling, indicating that CCL5 and CCR5 are key chemokine-related factors in atherogenesis. SMC proliferation and synthetic phenotype transformation attenuation by CCR5 pharmacological inhibition may offer a new approach to treatment or prevention of atherosclerotic diseases associated with hyperlipidemia.

(1) Background: While an artificial intelligence (AI)-based, cardiologist-level, deep-learning model for detecting acute myocardial infarction (AMI), based on a 12-lead electrocardiogram (ECG), has been established to have extraordinary capabilities, its real-world performance and clinical applications are currently unknown. (2) Methods and Results: To set up an artificial intelligence-based alarm strategy (AI-S) for detecting AMI, we assembled a strategy development cohort including 25,002 visits from August 2019 to April 2020 and a prospective validation cohort including 14,296 visits from May to August 2020 at an emergency department. The components of AI-S consisted of chest pain symptoms, a 12-lead ECG, and high-sensitivity troponin I. The primary endpoint was to assess the performance of AI-S in the prospective validation cohort by evaluating F-measure, precision, and recall. The secondary endpoint was to evaluate the impact on door-to-balloon (DtoB) time before and after AI-S implementation in STEMI patients treated with primary percutaneous coronary intervention (PPCI). Patients with STEMI were alerted precisely by AI-S (F-measure = 0.932, precision of 93.2%, recall of 93.2%). Strikingly, in comparison with pre-AI-S (N = 57) and post-AI-S (N = 32) implantation in STEMI protocol, the median ECG-to-cardiac catheterization laboratory activation (EtoCCLA) time was significantly reduced from 6.0 (IQR, 5.0–8.0 min) to 4.0 min (IQR, 3.0–5.0 min) (p < 0.01). The median DtoB time was shortened from 69 (IQR, 61.0–82.0 min) to 61 min (IQR, 56.8–73.2 min) (p = 0.037). (3) Conclusions: AI-S offers front-line physicians a timely and reliable diagnostic decision-support system, thereby significantly reducing EtoCCLA and DtoB time, and facilitating the PPCI process. Nevertheless, large-scale, multi-institute, prospective, or randomized control studies are necessary to further confirm its real-world performance.

Patients bitten by Naja atra who are treated with bivalent freeze-dried neurotoxic antivenom in Taiwan have an improved survival rate but develop necrotic wound changes. The World Health Organization (WHO) has suggested using the minimum necrotizing dose (MND) of venom as a method of evaluating the neutralization effect of antivenom. The aim of this study was to evaluate the effectiveness of antivenom for the prevention of necrosis based on the MND and clarify which component of the venom of N. atra induces necrosis. The neurotoxins (NTXs) were removed from the crude venom (deNTXs), and different concentrations of deNTXs were injected intradermally into the dorsal skin of mice. After three days, the necrotic lesion diameter was found to be approximately 5 mm, and the MND was calculated. A reduction in the necrotic diameter of 50% was used to identify the MND50. Furthermore, both phospholipase A2 (PLA2) and cytotoxins (CTXs) were separately removed from the deNTXs to identify the major necrosis-inducing factor, and the necrotic lesions were scored. All mice injected with deNTXs survived for three days and developed necrotic wounds. The MND of the deNTXs for mice was 0.494 ± 0.029 µg/g, that of the deNTXs-dePLA2 (major component retained: CTXs) was 0.294 ± 0.05 µg/g, and that of the deNTX-deCTX (major component retained: PLA2) venom was greater than 1.25 µg/g. These values show that CTX is the major factor inducing necrosis. These results suggest that the use of the deNTXs is necessary to enable the mice to survive long enough to develop venom-induced cytolytic effects. CTXs play a major role in N. atra-related necrosis. However, the MND50 could not be identified in this study, which meant that the antivenom did not neutralize venom-induced necrosis.

BACKGROUND:Diabetes is the most common comorbidity of necrotizing fasciitis (NF), but the effect of stress-induced hyperglycemia (SIH) on diabetic patients with NF has never been investigated. The aim of this study was to assess whether SIH, as determined by the glycemic gap between admission glucose levels and A1C-derived average glucose levels, predicts adverse outcomes in diabetic patients hospitalized with NF. METHODS:We retrospectively reviewed the glycemic gap and clinical outcomes in 252 diabetic patients hospitalized due to NF from 2011 to 2018 in a single medical center in Taiwan. A receiver operating characteristic (ROC) curve was used to analyze the optimal cutoff values for predicting adverse outcomes. Univariate and multivariate logistic regression analyses were employed to identify significant predictors of adverse outcomes. RESULTS:In total, 194 diabetic NF patients were enrolled. Compared with patients without adverse outcomes, patients with adverse outcomes had significantly higher glycemic gaps, Acute Physiology and Chronic Health Evaluation (APACHE) II scores and C-reactive protein (CRP) levels; lower albumin and hemoglobin levels; greater incidence of limb loss; and longer hospital and intensive care unit stays. The glycemic gap positively correlates with the laboratory risk indicator for NF scores, APACHE II scores and CRP levels. A glycemic gap of 146 mg/dL was the optimal cutoff value for predicting adverse outcomes using the ROC curve. Compared with patients with glycemic gaps ≤146 mg/dL, those with glycemic gaps >146 mg/dL had higher APACHE II scores and incidence rates of adverse outcomes, especially bacteremia and acute kidney injury. Multivariate analysis revealed that a glycemic gap >146 mg/dL and APACHE II score >15 were independent predictors of adverse outcomes, while the presence of hyperglycemia at admission was not. CONCLUSIONS:An elevated glycemic gap was significantly independently associated with adverse outcomes in diabetic NF patients. Further prospective studies are warranted to validate the role of the glycemic gap in NF patients with diabetes.

ObjectiveAortic calcification (AC) is associated with increased risks of cardiovascular events and mortality. Numerous studies have explored the association between calcification and abdominal artery aneurysm. However, evidence regarding the association between AC and acute aortic dissection (AAD) is limited. We aimed to evaluate the association between AC-related variables and the development of intimal tear (IT) in patients with AAD.MethodsWe conducted a retrospective observational study involving 64 patients with type A AAD and 32 patients with type B AAD from February, 2011 to January, 2017 at a tertiary referral medical center in Taiwan. We used the default analysis module "calcification score analysis" to calculate all the calcification variables, including AC scores and volume.ResultsWe identified an association between AC and AAD. Patients with AAD had a greater AC volume in the aortic arch and greater AC scores for both the ascending aorta and the aortic arch than did patients without AAD. However, hypertension and coronary artery disease, rather than AC remained to be the independent risk factor for AAD in multivariate analysis. Patients with type A AAD had greater mean and cumulative AC volumes in the aortic arch, greater cumulative AC volumes in the whole aorta and higher cumulative AC scores in the aortic arch than did patients with type B AAD. ACs were superimposed on ITs in nearly half of the patients with AAD. In patients with type A AAD, AC was more commonly located distal to the IT and farther from the IT.ConclusionsWe identified the associations between AC-related variables and the location of IT in patients with AAD. However, AC was not an independent risk factor for AAD. The distribution of AC was different between patients with type A and type B AAD.

BackgroundRecent studies have indicated that several critical illnesses are associated with an increased risk of cardiovascular diseases (CVDs). Nonetheless, studies of the association between heat-related illnesses (HRIs) and subsequent CVDs are still limited. We sought to evaluate whether heat stroke (HS) was associated with an increased CVD incidence.MethodsThe data from the nationwide, population-based, retrospective, cohort study described herein were obtained from the National Health Insurance Research Database in Taiwan. The outcome evaluated in this study was the cumulative incidence of CVDs, which was compared between patients with HS, patients with other HRIs and a control group during a 14-year follow-up period.ResultsOur analyses included 150 HS cases, 150 patients with other HRIs and 150 patients without HRIs. The HS patients had a significantly higher incidence of developing CVDs than the other HRI and control patients (32.67% vs. 23.33% vs. 16.67%, p = 0.005). Patients with HS had an increased incidence of acute myocardial infarction (AMI) compared with that of the controls (6% vs. 2.67%, p = 0.042) and an increased incidence of acute ischemic stroke (AIS) compared with those of the other HRI and control patients (12% vs. 6% vs. 4.67%, p = 0.038). An increased risk of chronic kidney disease (CKD) was also found in the patients with HS and other HRIs compared to that in the controls (17.33% vs. 14.67% vs. 6.67%, p = 0.016).ConclusionPrior HS was associated with an increased incidence of CVDs, particularly AMI and AIS, and an increased incidence of CKD.

The impact of the coronavirus disease 2019 (COVID-19) pandemic on health-care quality in the emergency department (ED) in countries with a low risk is unclear. This study aimed to explore the effects of the COVID-19 pandemic on ED loading, quality of care, and patient prognosis. Data were retrospectively collected from 1 January 2018 to 30 September 2020 at the ED of Tri-service general hospital. Analyses included day-based ED loading, quality of care, and patient prognosis. Data on triage assessment, physiological states, disease history, and results of laboratory tests were collected and analyzed. The number of daily visits significantly decreased after the pandemic, leading to a reduction in the time to examination. Admitted patients benefitted from the pandemic with a reduction of 0.80 h in the length of stay in the ED, faster discharge without death, and reduced re-admission. However, non-admitted visits with chest pain increased the risk of mortality after the pandemic. In conclusion, the COVID-19 pandemic led to a significant reduction in low-acuity ED visits and improved prognoses for hospitalized patients. However, clinicians should be alert about patients with chest pain due to their increased risk of mortality in subsequent admission.

The chain of survival has been shown to improve the chances of survival for victims of cardiac arrest. Post-cardiac arrest care has been demonstrated to significantly impact the survival of out-of-hospital cardiac arrest (OHCA). How post-cardiac arrest care influences the survival of OHCA patients has been a main concern in recent years. The objective of this study was to assess the survival outcome of hospitalized OHCA patients and determine the factors associated with improved survival in terms of survival to discharge. We conducted a retrospective observational study by analyzing records from the National Health Insurance Research Database of Taiwan from 2007 to 2013. We collected cases with an International Classification of Disease Clinical Modification, 9th revision primary diagnosis codes of 427.41 (ventricular fibrillation, VF) or 427.5 (cardiac arrest) and excluded patients less than 18 years old, as well as cases with an unknown outcome or a combination of traumatic comorbidities. We then calculated the proportion of survival to discharge among hospitalized OHCA patients. Factors associated with the dependent variable were examined by logistic regression. Statistical analysis was conducted using SPSS 22 (IBM, Armonk, NY). Of the 11,000 cases, 2,499 patients (22.7%) survived to hospital discharge. The mean age of subjects who survived to hospital discharge and those who did not was 66.7±16.7 and 71.7±15.2 years, respectively. After adjusting for covariates, neurological failure, cardiac comorbidities, hospital level, intensive care unit beds, transfer to another hospital, and length of hospital stay were independent predictors of improved survival. Cardiac rhythm on admission was a strong factor associated with survival to discharge (VF vs. non-VF: adjusted odds ratio: 3.51; 95% confidence interval: 3.06-4.01). In conclusion, cardiac comorbidities, hospital volume, cardiac rhythm on admission, transfer to another hospital and length of hospital stay had a significant positive association with survival to discharge in hospitalized OHCA patients in Taiwan.

Background: Medical students who graduate after 2003 need to participate in the "Postgraduate Primary Care Medical Training Program," provided by the Taiwan Joint Commission on Hospital Accreditation. We wish to know how the education and assignment strategy influences National Defense Medical Center (NDMC) graduates. We examined whether the performance of postgraduate year (PGY) trainees would be affected by the assignment strategies. Materials and Methods: We consecutively collected 173 NDMC graduated trainees who participated in 6-months of PGY training and another 94 trainees who participated for 1-year. During the training period, all the trainees were evaluated by several assessment tools. Trainees were dichotomized according to the levels of dispatched hospitals and preassigned specialty, respectively, to evaluate those effects on the performance of the 6-month PGY training period. Results: We describe the assessment scores of NDMC graduate M.D. trainees engaged in the Tri-Service General Hospital (TSGH) PGY training program. PGY trainees who were preassigned to TSGH due to better overall averages in medical school had better scores in case-based discussion, mini-clinical evaluation exercise, and direct observation of procedural skills than those who were preassigned to the Regional Teaching Hospitals. There was no statistically significant difference in the overall scores. The preassigned specialties themselves did not affect the performance in PGY training. Incorporation of PGY scores in the assignment strategy significantly elevated the performance of PGY trainees who were dispatched to TSGH. Conclusion: The accumulated PGY training database provides educators a unique opportunity in reviewing the effects of education policies and strategies. Assignment strategy could affect the performance of PGY trainees during their training period.

Purpose: Numerous studies have investigated the significant relationship between sciatic pain, radiating lower back pain, lumbosacral radicular syndrome or other disk disorders and cigarette smoking; however, only few reports have demonstrated the relationship between the total smoking dose and lumbar disk herniation (LDH), a cause of lower back or sciatic pain. Furthermore, the relationship between total cigarette consumption and the need of surgical intervention for LDH has not yet been investigated. Materials and Methods: This study included 391 patients with symptomatic LDH. The control group comprised 431 inpatients admitted for other medical or surgical problems. Their demographic data and level of cigarette consumption were obtained through a chart review. The association between lumbar surgical intervention and the clinical characteristics were investigated by multiple logistic regression analyses, with stepwise selection. Results: Compared with the nonsmokers, the smokers had a 1.5-fold increased risk of developing LDH (P = 0.01). An increased total smoking dose (pack-years) was a risk factor of undergoing lumbar surgical intervention among the LDH patients (odds ratio [OR] = 1.02; P = 0.03). Furthermore, the risk of undergoing lumbar surgical intervention increased to 1.83 times among LDH patients with a 6-10-year smoking history and to 2.16 times among those with >10-year smoking history (P = 0.02 and P = 0.002, respectively). Conclusion: This study found that the total cigarette smoking dose was associated with LDH and was a risk factor for undergoing surgical intervention for LDH.

Ventriculoperitoneal (VP) shunt is an established method of diverting cerebrospinal fluid for the management of hydrocephalus. The procedure is associated with various complications. Bowel perforation caused by migration of VP shunt is rare but serious complication. Because most of the patients are asymptomatic, and the occurrence of such complication is fatal due to ascending meningitis, early diagnosis, and rapid treatment is important in these patients. The diagnosis of such complication is based on direct visual of the protruding tube from the anus or abdominal computed tomography. Colon perforation due to shunt catheter migration may initially but not essentially present as meningitis after shunt infection, abdominal symptoms, seizure, and fever. However, colon perforation may rarely resemble the symptoms of acute gastroenteritis (abdominal pain, vomiting and/or diarrhea) before the prolapse of shunt catheter from the rectum. Here, we report a 75-year-old man underwent VP shunt for hydrocephalus presented with "watery diarrhea" masqueraded as acute gastroenteritis and further diagnosed as migration of VP shunt from the colon, via digital examination and further disclosed by computed tomography.

Pyogenic liver abscess (PLA) is a common intra-abdominal infection in immunocompromised patients. The disease is associated with a high mortality rate if not be diagnosed promptly. Fever may be the only sign of PLA and the disease is sometimes misdiagnosed because it is often asymptomatic. We report a 26-year-old male who presented with Klebsiella pneumoniae PLA 3 weeks after being treated for K. pneumoniae peritonsillar abscess. The K. pneumoniae PLA was diagnosed by abdominal ultrasound and treated with percutaneous drainage and an adequate period of antibiotic therapy. This case demonstrates the importance of considering K. pneumoniae PLA in immunocompetent patients who present with fever of unknown cause and recent K. pneumoniae infection.

Objective: To report two cases of recurrent uterine sarcoma that developed ifosfamide-induced encephalopathy (IIE) with successful management. Case Reports: The patient in the first case developed grade 4 toxicity and had a partial response after the fourth dose of intravenous methylene blue was administered. Full recovery occurred 4 days after the development of IIE. The patient in the second case, who had grade 3 toxicity, had completely recovered 32 hours after the first dose of thiamine. Conclusion: Careful evaluation of patients with recurrent gynecologic cancers and vigilance during infusion of chemotherapeutic regimens are important in reducing the risk and timely management of IIE. Both methylene blue and thiamine appear to be effective treatments for IIE.

PURPOSE: The purpose of this study was to determine the contribution of multidetector-row computed tomography (MDCT) in the management of adhesion-related small bowel obstruction (SBO) and to identify its predictive value for surgery. METHODS: We conducted a retrospective review of 151 patients over a 5-year period with the diagnosis of SBO caused by adhesion. These patients were divided into two groups: surgery (n = 63) and observation group (n = 88). Two radiologists blinded to the outcome of the patients evaluated MDCT images retrospectively, recording the bowel diameter, bowel wall thickness, degree of obstruction, air-fluid level, mesenteric fatty stranding, transitional zone, intraperitoneal fluid, close loop, whirl sign, and faeces sign. Statistical analyses were performed using univariate and multivariable analyses. RESULTS: Multivariable analysis showed that MDCT demonstrated presence of intraperitoneal fluid (Odds ratio, OR, 4.38), high-grade or complete obstruction (OR, 3.19) and mesenteric fatty stranding (OR, 2.81), and absence of faeces sign (OR, 2.11) were the most significant predictors. When all of the four criteria were used in combination, high sensitivity of 98.4% and specificity of 90.9% were achieved for the prediction for surgery. CONCLUSION: MDCT is useful to evaluate adhesion-related SBO and to predict accurately patients who require surgery. Use of the four MDCT features in combination is highly suggestive of the need for early surgical intervention.

OBJECTIVES: To assess whether chronic glycemic control and stress-induced hyperglycemia, determined by the gap between admission glucose levels and A1C-derived average glucose (ADAG) levels adversely affects outcomes in diabetic patients with pyogenic liver abscess (PLA). METHODS: Clinical, laboratory, and multi-detector computed tomography (MDCT) findings of 329 PLA patients (2004-2010) were retrospectively reviewed. HbA1C levels were used to determine long-term glycemic control status, which were then converted to estimated average glucose values. For the gap between admission glucose levels and ADAG levels, we used receiver operating characteristic (ROC) curve to determine the optimal cut-off values predicting adverse outcomes. Univariate and multivariate logistic regressions were used to identify predictors of adverse outcomes. RESULTS: Diabetic PLA patients with poorer glycemic control had significantly higher Klebsiella pneumoniae (KP) infection rates, lower albumin levels, and longer hospital stays than those with suboptimal and good glycemic control. The ROC curve showed that a glycemic gap of 72 mg/dL was the optimal cut-off value for predicting adverse outcomes and showed a 22.3% relative increase in adverse outcomes compared with a glycemic gap

Bisphosphonates are a class of pharmacologic compounds that are commonly used to treat postmenopausal osteoporosis and malignant osteolytic processes. Studies have shown that bone marrow-derived endothelial progenitor cells (EPCs) play a significant role in postnatal neovascularization. Whether the nitrogen-containing bisphosphonate zoledronate inhibits ischemia-induced neovascularization by modulating EPC functions remains unclear.Unilateral hindlimb ischemia was surgically induced in wild-type mice after 2 weeks of treatment with vehicle or zoledronate (low-dose: 30 μg/kg; high-dose: 100 μg/kg). Doppler perfusion imaging demonstrated that the ischemic limb/normal side blood perfusion ratio was significantly lower in wild-type mice treated with low-dose zoledronate and in mice treated with high-dose zoledronate than in controls 4 weeks after ischemic surgery (control vs. low-dose vs. high-dose: 87±7% vs. *61±18% vs. **49±17%, *p