The Association between Disseminated Intravascular Coagulation Profiles and Neurologic Outcome in Patients with In-Hospital Cardiac Arrest.

Background: The relationship between disseminated intravascular coagulation (DIC) profiles and survival or neurological outcomes in out-of-hospital cardiac arrest (OHCA) patients is well known. In contrast, the relationship between DIC profiles and neurological outcomes in patients with in-hospital cardiac arrest (IHCA) remains unclear. This study sought to examine the correlation between DIC profiles and neurological outcomes in IHCA patients. Methods: A retrospective observational study was conducted on comatose adult IHCA patients treated with targeted temperature management between January 2017 and December 2022. DIC profiles were used to calculate the DIC score, and were measured immediately after the return of spontaneous circulation (ROSC). The primary endpoint was a poor neurological outcome at six months, defined by cerebral performance in categories 3, 4, or 5. Multivariate analysis was used to evaluate the association between DIC profiles and poor neurological outcomes. Results: The study included 136 patients, of which 107 (78.7%) patients demonstrated poor neurological outcomes. These patients had higher fibrinogen (3.2 g/L vs. 2.3 g/L) and fibrin degradation product levels (50.7 mg/L vs. 30.1 mg/L) and lower anti-thrombin III (ATIII) levels (65.7% vs. 82.3%). The DIC score did not differ between the good and poor outcome groups. In multivariable analysis, fibrinogen (odds ratio [OR], 1.009; 95% confidence intervals [CI], 1.003-1.016) and ATIII levels (OR, 0.965; 95% CI, 0.942-0.989) were independently associated with poor neurological outcomes. Conclusions: Decreased fibrinogen and ATIII levels after ROSC were an independent risk factor for unfavorable neurological outcomes in IHCA. The DIC score is unlikely to play a significant role in IHCA prognosis in contrast to OHCA.

Sphingolipid metabolites as potential circulating biomarkers for sarcopenia in men.

BACKGROUND: Sarcopenia is an age-related progressive loss of muscle mass and function. Sarcopenia is a multifactorial disorder, including metabolic disturbance; therefore, metabolites may be used as circulating biomarkers for sarcopenia. We aimed to investigate potential biomarkers of sarcopenia using metabolomics. METHODS: After non-targeted metabolome profiling of plasma from mice of an aging mouse model of sarcopenia, sphingolipid metabolites and muscle cells from the animal model were evaluated using targeted metabolome profiling. The associations between sphingolipid metabolites identified from mouse and cell studies and sarcopenia status were assessed in men in an age-matched discovery (72 cases and 72 controls) and validation (36 cases and 128 controls) cohort; women with sarcopenia (36 cases and 36 controls) were also included as a discovery cohort. RESULTS: Both non-targeted and targeted metabolome profiling in the experimental studies showed an association between sphingolipid metabolites, including ceramides (CERs) and sphingomyelins (SMs), and sarcopenia. Plasma SM (16:0), CER (24:1), and SM (24:1) levels in men with sarcopenia were significantly higher in the discovery cohort than in the controls (all P < 0.05). There were no significant differences in plasma sphingolipid levels for women with or without sarcopenia. In men in the discovery cohort, an area under the receiver-operating characteristic curve (AUROC) of SM (16:0) for low muscle strength and low muscle mass was 0.600 (95% confidence interval [CI]: 0.501-0.699) and 0.647 (95% CI: 0.557-0.737). The AUROC (95% CI) of CER (24:1) and SM (24:1) for low muscle mass in men was 0.669 (95% CI: 0.581-0.757) and 0.670 (95% CI: 0.582-0.759), respectively. Using a regression equation combining CER (24:1) and SM (16:0) levels, a sphingolipid (SphL) score was calculated; an AUROC of the SphL score for sarcopenia was 0.712 (95% CI: 0.626-0.798). The addition of the SphL score to HGS significantly improved the AUC from 0.646 (95% CI: 0.575-0.717; HGS only) to 0.751 (95% CI: 0.671-0.831, P = 0.002; HGS + SphL) in the discovery cohort. The predictive ability of the SphL score for sarcopenia was confirmed in the validation cohort (AUROC = 0.695, 95% CI: 0.591-0.799). CONCLUSIONS: SM (16:0), reflecting low muscle strength, and CER (24:1) and SM (16:0), reflecting low muscle mass, are potential circulating biomarkers for sarcopenia in men. Further research on sphingolipid metabolites is required to confirm these results and provide additional insights into the metabolomic changes relevant to the pathogenesis and diagnosis of sarcopenia.

Comparative analysis of body composition using torso CT from PET/CT with bioelectrical impedance and muscle strength in healthy adults.

The role of torso computed tomography (CT) in evaluating body composition has been unexplored. This study assessed the potential of low-dose torso CT from positron emission tomography (PET)/CT for analyzing body composition and its relation to muscle strength. We retrospectively recruited 384 healthy Korean adults (231 men, 153 women) who underwent torso 18F-FDG PET/CT, bioelectrical impedance analysis (BIA), and muscle strength tests (handgrip strength [HGS] and knee extension strength [KES]). CT images were segmented into three compartments: torso volumetric, abdominal volumetric, and abdominal areal. Muscle amounts from each compartment were indexed to height (m2). BIA and HGS served as reference standards, with correlation coefficients (r) calculated. Torso muscle volumetric index (TorsoMVI) had the strongest correlations with BIA-derived values (r = 0.80 for men; r = 0.73 for women), surpassing those from the abdominal compartments. TorsoMVI was also correlated significantly with HGS (r = 0.39, p < 0.01) and differentiated between normal and possible sarcopenia in men (n = 225, 5960 ± 785 cm3/m2 vs. n = 6, 5210 ± 487 cm3/m2, p = 0.02). In women, KES correlated more strongly with muscle parameters than HGS. Despite gender-specific variations, torso CT-derived parameters show promise for evaluating body composition and sarcopenia.

Lactate to albumin ratio as a prognosis predictor in gastrointestinal bleeding in the emergency department.

Gastrointestinal bleeding (GIB) is a common cause of emergency department (ED) visits, and has various prognoses. This study aimed to verify the prognostic ability of the lactate/albumin (L/A) ratio in patients with GIB compared with the AIMS65 score and blood urea nitrogen/albumin (B/A) ratio. This retrospective study included patients with GIB symptoms who visited the ED in 2019. Baseline characteristics and laboratory data were obtained to calculate the L/A and B/A ratios and AIMS65 score. Each score was evaluated as a predictor of intensive care unit (ICU) admission and in-hospital mortality by using the area under the receiver operating characteristic (AUROC) curve. The multivariate logistic regression analysis revealed that the L/A ratio significantly predicted ICU admission and in-hospital mortality. The AUROC curve for predicting ICU admission were 0.788, 0.695, and 0.586 for the L/A, B/A, and AIMS65 scores, respectively, while the AUROC curve for predicting in-hospital mortality were 0.807, 0.799, and 0.683 for the L/A, B/A, and AIMS65 scores, respectively. The L/A ratio, which consists of the serum lactate and albumin levels, showed superior performance relative to the B/A ratio and AIMS65 score in predicting the prognosis of patients with GIB.

The Relationship between the Ratio of Urine Osmolality to Serum Osmolality and Neurological Outcomes in Out-of-hospital Cardiac Arrest Patients.

Background: Progressive ischemic brain injury after cardiac arrest can cause damage to the hypothalamic-pituitary axis, particularly the pituitary gland. This may impact serum osmolality (SOsm) and urine osmolality (UOsm) in patients who have experienced out-of-hospital cardiac arrest (OHCA). We assumed that a low ratio of UOsm to SOsm (USR) is related to poor outcomes among OHCA patients. Therefore, the present study was designed to evaluate the association between the USR within 72 h after the restoration of spontaneous circulation (ROSC) and 6-month neurological outcomes in OHCA patients. Methods: This prospective, observational study included OHCA patients with targeted temperature management at Chonnam National University Hospital in Gwangju, Korea, between January 2016 and December 2022. We collected SOsm and UOsm data at admission (T0) and 24 (T1), 48 (T2), and 72 h (T3) after ROSC. The primary outcome was a poor neurological outcome at 6 months defined by cerebral performance categories 3, 4, or 5. Results: This study included 319 patients. The mean UOsm and USRs at T0, T1, T2, and T3 of patients with poor outcomes were lower than those of patients with good outcomes. Multivariable analysis indicated that the USRs at T1 (odds ratio [OR], 0.363; 95% confidence interval [CI], 0.221-0.594), T2 (OR, 0.451; 95% CI, 0.268-0.761), and T3 (OR, 0.559; 95% CI, 0.357-0.875) were associated with a poor outcome. The areas under the receiver operating characteristic curves of USRs at T0, T1, T2, and T3 for predicting poor outcomes were 0.615 (95% CI, 0.559-0.669), 0.711 (95% CI, 0.658-0.760), 0.724 (95% CI, 0.671-0.772), and 0.751 (95% CI, 0.699-0.797), respectively. Conclusions: The USRs within 72 h of ROSC were associated with poor neurological outcomes at 6 months in OHCA patients.

Validation of the Korean Version of the Clinical Frailty Scale-Adjusted Korean Triage and Acuity Scale for Older Patients in the Emergency Department.

Background and Objectives: The Clinical Frailty Scale (CFS), used to screen for prehospital frailty in patients aged >65 years, is simple, time-efficient, and has been validated in emergency departments (EDs). In this study, we analyzed whether the Korean Triage and Acuity Scale (KTAS) classification by level in older patients determined to have frailty based on the Korean version of the CFS increases the triage performance of the current KTAS. Materials and Methods: The primary outcome was 30-day in-hospital mortality, and secondary outcomes were hospital and intensive care unit (ICU) admissions. This study retrospectively analyzed prospectively collected data from three ED centers. Patients with a CFS score ranging from five (mildly frail) to nine (terminally ill) were categorized into the frailty group. We upgraded the KTAS classification of the frailty group by one level of urgency and defined this as the CFS-KTAS. Results: The cutoff values for predicting admission were three and two for the KTAS and CFS-KTAS, respectively. A significant difference was observed in the area under the receiver operating characteristic (AUROC) curve between the KTAS and CFS-KTAS. To predict ICU admission, the cutoff score was two for both scales. A significant difference was observed in the AUROC curve between the KTAS and CFS-KTAS. For predicting in-hospital mortality, the cutoff score was two for both scales. A significant difference was observed in the AUROC curve between the KTAS and CFS-KTAS. Conclusions: This study showed that the CFS-adjusted KTAS has a more useful prognostic value than the KTAS alone for predicting hospital outcomes in older patients.

Targeting pyruvate dehydrogenase kinase 1 overcomes EGFR C797S mutation-driven osimertinib resistance in non-small cell lung cancer.

Osimertinib, a selective third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), effectively targets the EGFR T790M mutant in non-small cell lung cancer (NSCLC). However, the newly identified EGFR C797S mutation confers resistance to osimertinib. In this study, we explored the role of pyruvate dehydrogenase kinase 1 (PDK1) in osimertinib resistance. Patients exhibiting osimertinib resistance initially displayed elevated PDK1 expression. Osimertinib-resistant cell lines with the EGFR C797S mutation were established using A549, NCI-H292, PC-9, and NCI-H1975 NSCLC cells for both in vitro and in vivo investigations. These EGFR C797S mutant cells exhibited heightened phosphorylation of EGFR, leading to the activation of downstream oncogenic pathways. The EGFR C797S mutation appeared to increase PDK1-driven glycolysis through the EGFR/AKT/HIF-1α axis. Combining osimertinib with the PDK1 inhibitor leelamine helped successfully overcome osimertinib resistance in allograft models. CRISPR-mediated PDK1 knockout effectively inhibited tumor formation in xenograft models. Our study established a clear link between the EGFR C797S mutation and elevated PDK1 expression, opening new avenues for the discovery of targeted therapies and improving our understanding of the roles of EGFR mutations in cancer progression.

Morroniside Protects C2C12 Myoblasts from Oxidative Damage Caused by ROS-Mediated Mitochondrial Damage and Induction of Endoplasmic Reticulum Stress.

Oxidative stress contributes to the onset of chronic diseases in various organs, including muscles. Morroniside, a type of iridoid glycoside contained in Cornus officinalis, is reported to have advantages as a natural compound that prevents various diseases. However, the question of whether this phytochemical exerts any inhibitory effect against oxidative stress in muscle cells has not been well reported. Therefore, the current study aimed to evaluate whether morroniside can protect against oxidative damage induced by hydrogen peroxide (H2O2) in murine C2C12 myoblasts. Our results demonstrate that morroniside pretreatment was able to inhibit cytotoxicity while suppressing H2O2-induced DNA damage and apoptosis. Morroniside also significantly improved the antioxidant capacity in H2O2-challenged C2C12 cells by blocking the production of cellular reactive oxygen species and mitochondrial superoxide and increasing glutathione production. In addition, H2O2-induced mitochondrial damage and endoplasmic reticulum (ER) stress were effectively attenuated by morroniside pretreatment, inhibiting cytoplasmic leakage of cytochrome c and expression of ER stress-related proteins. Furthermore, morroniside neutralized H2O2-mediated calcium (Ca2+) overload in mitochondria and mitigated the expression of calpains, cytosolic Ca2+-dependent proteases. Collectively, these findings demonstrate that morroniside protected against mitochondrial impairment and Ca2+-mediated ER stress by minimizing oxidative stress, thereby inhibiting H2O2-induced cytotoxicity in C2C12 myoblasts.

Predictors for emergency readmission in patients with ureteral calculi: a focus on pain management and stone location.

BACKGROUND: The management of patients with ureteral calculi in the emergency department (ED) remains challenging due to high revisit rates. PURPOSE: To identify predictors of revisits among patients with ureteral calculi in the ED. DESIGN, SETTING, AND PARTICIPANTS: Data from patients who presented at a tertiary academic hospital in Seoul, Republic of Korea, between February 2018 and December 2019, were analyzed retrospectively. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Variables, including the respiratory rate (RR), estimated glomerular filtration rate (eGFR), duration of pain, number of analgesic doses, location of ureteral calculi, and ED length of stay (LOS) were examined using logistic regression. We also examined some additional variables included in the STONE and CHOKAI scoring systems to examine their association with revisit. RESULTS: Significant predictors of revisits included the number of analgesic doses and the location of ureteral calculi. Patients who required multiple analgesic doses or those with proximal or mid-ureteral calculi were more likely to revisit the ED. Although the STONE and CHOKAI scores could predict uncomplicated ureteral calculi, we found that the CHOKAI score is a valuable tool for predicting the likelihood of patient revisits (p = 0.021). CONCLUSIONS: Effective pain management and consideration of calculi location are important for predicting patient revisits. More research is required to validate findings, develop precise predictive models, and empower tailored care for high-risk patients. In patients with ureteral calculi in the ED, the number of analgesics given and stone location predict return visits. Proximal ureteral calculi on CT may require early urologic intervention to prevent pain-related revisits.

NINJ1 mediates inflammatory cell death, PANoptosis, and lethality during infection conditions and heat stress.

Innate immunity provides the first line of defense through multiple mechanisms, including pyrogen production and cell death. While elevated body temperature during infection is beneficial to clear pathogens, heat stress (HS) can lead to inflammation and pathology. Links between pathogen exposure, HS, cytokine release, and inflammation have been observed, but fundamental innate immune mechanisms driving pathology during pathogen exposure and HS remain unclear. Here, we use multiple genetic approaches to elucidate innate immune pathways in infection or LPS and HS models. Our results show that bacteria and LPS robustly increase inflammatory cell death during HS that is dependent on caspase-1, caspase-11, caspase-8, and RIPK3 through the PANoptosis pathway. Caspase-7 also contributes to PANoptosis in this context. Furthermore, NINJ1 is an important executioner of this cell death to release inflammatory molecules, independent of other pore-forming executioner proteins, gasdermin D, gasdermin E, and MLKL. In an in vivo HS model, mortality is reduced by deleting NINJ1 and fully rescued by deleting key PANoptosis molecules. Our findings suggest that therapeutic strategies blocking NINJ1 or its upstream regulators to prevent PANoptosis may reduce the release of inflammatory mediators and benefit patients.

Natural Product-Based Glycolysis Inhibitors as a Therapeutic Strategy for Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor-Resistant Non-Small Cell Lung Cancer.

Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related deaths worldwide. Targeted therapy against the epidermal growth factor receptor (EGFR) is a promising treatment approach for NSCLC. However, resistance to EGFR tyrosine kinase inhibitors (TKIs) remains a major challenge in its clinical management. EGFR mutation elevates the expression of hypoxia-inducible factor-1 alpha to upregulate the production of glycolytic enzymes, increasing glycolysis and tumor resistance. The inhibition of glycolysis can be a potential strategy for overcoming EGFR-TKI resistance and enhancing the effectiveness of EGFR-TKIs. In this review, we specifically explored the effectiveness of pyruvate dehydrogenase kinase inhibitors and lactate dehydrogenase A inhibitors in combating EGFR-TKI resistance. The aim was to summarize the effects of these natural products in preclinical NSCLC models to provide a comprehensive understanding of the potential therapeutic effects. The study findings suggest that natural products can be promising inhibitors of glycolytic enzymes for the treatment of EGFR-TKI-resistant NSCLC. Further investigations through preclinical and clinical studies are required to validate the efficacy of natural product-based glycolytic inhibitors as innovative therapeutic modalities for NSCLC.

Inhibition of SIRT7 overcomes sorafenib acquired resistance by suppressing ERK1/2 phosphorylation via the DDX3X-mediated NLRP3 inflammasome in hepatocellular carcinoma.

AIMS: Sirtuin 7 (SIRT7) plays an important role in tumor development, and has been characterized as a potent regulator of cellular stress. However, the effect of SIRT7 on sorafenib acquired resistance remains unclear and a possible anti-tumor mechanism beyond this process in HCC has not been clarified. We examined the therapeutic potential of SIRT7 and determined whether it functions synergistically with sorafenib to overcome chemoresistance. METHODS: Cancer Genome Atlas-liver HCC data and unbiased gene set enrichment analyses were used to identify SIRT7 as a potential effector molecule in sorafenib acquired resistance. Two types of SIRT7 chemical inhibitors were developed to evaluate its therapeutic properties when synergized with sorafenib. Mass spectrometry was performed to discover a direct target of SIRT7, DDX3X, and DDX3X deacetylation levels and protein stability were explored. Moreover, an in vivo xenograft model was used to confirm anti-tumor effect of SIRT7 and DDX3X chemical inhibitors combined with sorafenib. RESULTS: SIRT7 inhibition mediated DDX3X depletion can re-sensitize acquired sorafenib resistance by disrupting NLRP3 inflammasome assembly, finally suppressing hyperactive ERK1/2 signaling in response to NLRP3 inflammasome-mediated IL-1ß inhibition. CONCLUSIONS: SIRT7 is responsible for sorafenib acquired resistance, and its inhibition would be beneficial when combined with sorafenib by suppressing hyperactive pro-cell survival ERK1/2 signaling.

Central 5-HTergic hyperactivity induces myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)-like pathophysiology.

OBJECTIVES: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a significant medical challenge, with no indisputable pathophysiological mechanism identified to date. METHODS: Based on clinical clues, we hypothesized that 5-hydroxytryptamine (5-HT) hyperactivation is implicated in the pathogenic causes of ME/CFS and the associated symptoms. We experimentally evaluated this hypothesis in a series of mouse models. RESULTS: High-dose selective serotonin reuptake inhibitor (SSRI) treatment induced intra- and extracellular serotonin spillover in the dorsal raphe nuclei of mice. This condition resulted in severe fatigue (rota-rod, fatigue rotating wheel and home-cage activity tests) and ME/CFS-associated symptoms (nest building, plantar and open field test), along with dysfunction in the hypothalamic-pituitary-adrenal (HPA) axis response to exercise challenge. These ME/CFS-like features induced by excess serotonin were additionally verified using both a 5-HT synthesis inhibitor and viral vector for Htr1a (5-HT1A receptor) gene knockdown. CONCLUSIONS: Our findings support the involvement of 5-HTergic hyperactivity in the pathophysiology of ME/CFS. This ME/CFS-mimicking animal model would be useful for understanding ME/CFS biology and its therapeutic approaches.

Regulated cell death pathways and their roles in homeostasis, infection, inflammation, and tumorigenesis.

Pyroptosis, apoptosis, necroptosis, and ferroptosis, which are the most well-studied regulated cell death (RCD) pathways, contribute to the clearance of infected or potentially neoplastic cells, highlighting their importance in homeostasis, host defense against pathogens, cancer, and a wide range of other pathologies. Although these four RCD pathways employ distinct molecular and cellular processes, emerging genetic and biochemical studies have suggested remarkable flexibility and crosstalk among them. The crosstalk among pyroptosis, apoptosis and necroptosis pathways is more evident in cellular responses to infection, which has led to the conceptualization of PANoptosis. In this review, we provide a brief overview of the molecular mechanisms of pyroptosis, apoptosis, necroptosis, and ferroptosis and their importance in maintaining homeostasis. We discuss the intricate crosstalk among these RCD pathways and the current evidence supporting PANoptosis, focusing on infectious diseases and cancer. Understanding the fundamental processes of various cell death pathways is crucial to inform the development of new therapeutics against many diseases, including infection, sterile inflammation, and cancer.

Diversity and complexity of cell death: a historical review.

Death is the inevitable fate of all living organisms, whether at the individual or cellular level. For a long time, cell death was believed to be an undesirable but unavoidable final outcome of nonfunctioning cells, as inflammation was inevitably triggered in response to damage. However, experimental evidence accumulated over the past few decades has revealed different types of cell death that are genetically programmed to eliminate unnecessary or severely damaged cells that may damage surrounding tissues. Several types of cell death, including apoptosis, necrosis, autophagic cell death, and lysosomal cell death, which are classified as programmed cell death, and pyroptosis, necroptosis, and NETosis, which are classified as inflammatory cell death, have been described over the years. Recently, several novel forms of cell death, namely, mitoptosis, paraptosis, immunogenic cell death, entosis, methuosis, parthanatos, ferroptosis, autosis, alkaliptosis, oxeiptosis, cuproptosis, and erebosis, have been discovered and advanced our understanding of cell death and its complexity. In this review, we provide a historical overview of the discovery and characterization of different forms of cell death and highlight their diversity and complexity. We also briefly discuss the regulatory mechanisms underlying each type of cell death and the implications of cell death in various physiological and pathological contexts. This review provides a comprehensive understanding of different mechanisms of cell death that can be leveraged to develop novel therapeutic strategies for various diseases.

Comparison of antibiotic resistance rates and outcomes among older adult patients with urinary tract infections living in long- term care hospitals and the community.

OBJECTIVE: In this study, we compared the proportion of antibiotic resistance between patients who visited the emergency department (ED) with urinary tract infection (UTI) from long-term care hospitals (LTCH), which is a type of long-term care facilities (LTCF) and the community. We assessed the resulting difference in prognosis. METHOD: Older adults who visited the ED between January and December 2019 and were diagnosed with UTI were divided into community residents and LTCH residents. We investigated the antibiotics sensitivity rates, end of therapy (EOT), and the patient's outcomes were evaluated. RESULTS: The antibiotic resistance rate was higher in LTCH residents. LTCH residents had a higher in hospital mortality rate compared to community residents. EOT was found to be longer, and admission rate and in-hospital mortality rate were also higher in LTCH residents. CONCLUSION: LTCF residents had a higher rate of antibiotic resistance and a poor prognosis.

Diagnosis of osteoporotic vertebral compression fractures and fracture level detection using multitask learning with U-Net in lumbar spine lateral radiographs.

Recent studies of automatic diagnosis of vertebral compression fractures (VCFs) using deep learning mainly focus on segmentation and vertebral level detection in lumbar spine lateral radiographs (LSLRs). Herein, we developed a model for simultaneous VCF diagnosis and vertebral level detection without using adjacent vertebral bodies. In total, 1102 patients with VCF, 1171 controls were enrolled. The 1865, 208, and 198 LSLRS were divided into training, validation, and test dataset. A ground truth label with a 4-point trapezoidal shape was made based on radiological reports showing normal or VCF at some vertebral level. We applied a modified U-Net architecture, in which decoders were trained to detect VCF and vertebral levels, sharing the same encoder. The multi-task model was significantly better than the single-task model in sensitivity and area under the receiver operating characteristic curve. In the internal dataset, the accuracy, sensitivity, and specificity of fracture detection per patient or vertebral body were 0.929, 0.944, and 0.917 or 0.947, 0.628, and 0.977, respectively. In external validation, those of fracture detection per patient or vertebral body were 0.713, 0.979, and 0.447 or 0.828, 0.936, and 0.820, respectively. The success rates were 96 % and 94 % for vertebral level detection in internal and external validation, respectively. The multi-task-shared encoder was significantly better than the single-task encoder. Furthermore, both fracture and vertebral level detection was good in internal and external validation. Our deep learning model may help radiologists perform real-life medical examinations.

Association of Visceral Fat Obesity, Sarcopenia, and Myosteatosis with Non-Alcoholic Fatty Liver Disease without Obesity.

BACKGROUND/AIMS: To investigate whether non-alcoholic fatty liver disease (NAFLD) in individuals without generalized obesity is associated with visceral fat obesity (VFO), sarcopenia, and/or myosteatosis. METHODS: This cross-sectional analysis included 14,400 individuals (7,470 men) who underwent abdominal computed tomography scans during routine health examinations. The total abdominal muscle area (TAMA) and skeletal muscle area (SMA) at the 3rd lumbar vertebral level were measured. The SMA was divided into the normal attenuation muscle area (NAMA) and low attenuation muscle area, and the NAMA/TAMA index was calculated. VFO was defined by visceral to subcutaneous fat ratio, sarcopenia by body mass index-adjusted SMA, and myosteatosis by the NAMA/TAMA index. NAFLD was diagnosed with ultrasonography. RESULTS: Of the 14,400 individuals, 4,748 (33.0%) had NAFLD, and the prevalence of NAFLD among non-obese individuals was 21.4%. In regression analysis, both sarcopenia (men: odds ratio [OR] 1.41, 95% confidence interval [CI] 1.19-1.67, P<0.001; women: OR=1.59, 95% CI 1.40-1.90, P<0.001) and myosteatosis (men: OR=1.24, 95% CI 1.02-1.50, P=0,028; women: OR=1.23, 95% CI 1.04-1.46, P=0.017) were significantly associated with non-obese NAFLD after considering for VFO and other various risk factors, whereas VFO (men: OR=3.97, 95% CI 3.43-4.59 [adjusted for sarcopenia], OR 3.98, 95% CI 3.44-4.60 [adjusted for myosteatosis]; women: OR=5.42, 95% CI 4.53-6.42 [adjusted for sarcopenia], OR=5.33, 95% CI 4.51-6.31 [adjusted for myosteatosis]; all P<0.001) was strongly associated with non-obese NAFLD after adjustment with various known risk factors. CONCLUSION: In addition to VFO, sarcopenia and/or myosteatosis were significantly associated with non-obese NAFLD.

Risk factors for deep neck infection in patients with sore throat and neck pain.

BACKGROUND: Deep neck infection (DNI) is a potentially life-threatening disease because infections spread quickly, causing se-rious complications. Therefore, more attention is needed than other neck infections, but there are many difficulties due to isolation guidelines in the period of coronavirus disease 2019 pandemic. We investigated the early predictability of DNI through patient symptoms at the first emergency department encounter. METHODS: This was a retrospective study of patients with suspected soft-tissue neck infections from January 2016 to February 2021. Symptoms were retrospectively analyzed in fever, foreign body sensation, chest discomfort/pain, submandibular pain, odynopha-gia, dysphagia, voice change, and severe pain. Furthermore, baseline characteristic data, laboratory findings, and pre-vertebral soft-tissue (PVST) thickness were evaluated. DNI and other neck infections were diagnosed through computed tomography. Logistic regression analysis was conducted to determine the independent factors for predicting DNI. RESULTS: In the 793 patients included in the study, 267 (33.7%) were diagnosed with DNI, and 526 (66.3%) were diagnosed with other soft-tissue neck infections. In the comparison between the two groups, C-reactive protein (CRP), sodium, PT (INR), foreign body sensation, chest discomfort/pain, submandibular pain, odynophagia, dysphagia, severe pain, and PVST thickness showed statisti-cally significant differences. Independent factors for predicting DNI were severe pain (odds ratio: 6.336 [3.635-11.045], p<0.001), for-eign body sensation (odds ratio: 7.384 [2.776-19.642], p<0.001), submandibular pain (odds ratio: 4.447 [2.852-6.932], p<0.001), and dysphagia (odds ratio: 52.118 [8.662-313.588], p<0.001) among symptoms and CRP (odds ratio: 1.034 [1.004-1.065], p=0.026) and PT (INR) (odds ratio: 29.660 [3.363-261.598], p=0.002) in laboratory tests. PVST thickness at C2 (odds ratio: 1.953 [1.609-2.370], p<0.001) and C6 level (odds ratio: 1.179 [1.054-1.319], p=0.004) was also shown as an independent variable for prediction. CONCLUSION: Among patients with sore throat or neck pain, patients with dysphagia, foreign body sensation, severe pain, and submandibular pain are more likely to have DN. DNI can cause serious complications; therefore, patients with the above symptoms should be closely observed due to the potential for significant complications.