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BackgroundCurrently, there is no consensus on the number of defibrillation attempts that should be made before transfer to a hospital in patients with out-of-hospital cardiac arrest (OHCA). This study aimed to evaluate the association between the number of defibrillations and a sustained prehospital return of spontaneous circulation (ROSC).MethodsA retrospective analysis of a multicentre, prospectively collected, registry-based study in Republic of Korea was conducted for OHCA patients with prehospital defibrillation. The primary outcome was sustained prehospital ROSC, and the secondary outcome was a good neurological outcome at hospital discharge, defined as Cerebral Performance Category score 1 or 2. Cumulative incidence of sustained prehospital ROSC and good neurological outcome according to number of defibrillations were examined. Multivariable logistic regression analysis was used to examine whether the number of defibrillations was independently associated with the outcomes.ResultsExcluding 172 patients with missing data, a total of 1983 OHCA patients who received prehospital defibrillation were included. The median time from arrest to first defibrillation was 10 (IQR 7–15) min. The numbers of patients with sustained prehospital ROSC and good neurological outcome were 738 (37%) and 549 (28%), respectively. Sustained ROSC rates decreased as the number of defibrillation attempts increased from the first to the sixth (16%, 9%, 5%, 3%, 2% and 1%, respectively). The cumulative sustained ROSC rate, and good neurological outcome rate from initial defibrillation to sixth defibrillation were 16%, 25%, 30%, 34%, 36%, 36% and 11%, 18%, 22%, 25%, 26%, 27%, respectively. With adjustment for clinical characteristics and time to defibrillation, a higher number of defibrillations was independently associated with a lower chance of a sustained ROSC (OR 0.81, 95% CI 0.76 to 0.86) and a lower chance of good neurological outcome (OR 0.86, 95% CI 0.80 to 0.92).ConclusionsWe observed no significant increase in ROSC after five defibrillations, and no absolute increase in ROSC after seven defibrillations. These data provide a starting point for determination of the optimal defibrillation strategy prior to consideration for prehospital extracorporeal cardiopulmonary resuscitation (ECPR) or conveyance to a hospital with an ECPR capability.Trial registration numberNCT03222999

Vitamin D is an important immune modulator and is associated with susceptibility to infection. However, past studies have reported inconsistent results regarding the association between vitamin D deficiency and mortality in patients with sepsis, and early-stage data regarding septic shock are limited. This study aimed to determine the relationship between vitamin D deficiency on admission to the emergency department (ED) and mortality in patients with septic shock.We analyzed prospectively collected data on adult patients with septic shock who were treated with protocol-driven resuscitation bundle therapy in the ED between September 2019 and February 2021. Septic shock was defined by the sepsis-3 definition and vitamin D deficiency was defined as a 25-hydroxyvitamin D20 ng/ml. The primary outcome was 30-day mortality.A total of 302 patients were included, 236 (78.1%) patients had vitamin D deficiency; it was significantly higher in non-survivors than in survivors (89.3% vs. 73.9%, P=0.004). Mortality was higher in vitamin D deficient patients than in non-deficient patients (31.8% vs. 13.6%, P=0.004). In multivariate analysis, vitamin D deficiency (odds ratio [OR], 2.43; 95 % confidence interval [CI], 1.03-5.74), hyperlactatemia (OR, 3.65; 95 % CI, 1.95-6.83), Sequential Organ Failure Assessment scores (OR, 1.22; 95% CI, 1.09-1.36), and albumin levels (OR, 0.39; 95% CI, 0.21-0.73) were significantly associated with 30-day mortality.Vitamin D deficiency was prevalent in patients with septic shock visiting the ED and was associated with mortality.

Purpose: This study was conducted to assess the antidepressant effects of capsaicin in chronic depressive rats and elucidate the mechanism underlying its effects.Methods: Male Wistar rats (280~320 g, 8 weeks of age) were subjected to depression induced by chronic unpredictable mild stresses. The rats were exposed to 8 kinds of stresses for 8 weeks. In the last 2 weeks, fluoxetine or capsaicin was injected subcutaneously. The dose of fluoxetine was 10 mg/kg (body weight), while the doses of capsaicin consisted of low (1 mg/kg), middle (5 mg/kg), and high (10 mg/kg). The forced swim test (FST) was conducted to evaluate the immobility time of rats. The immobility time indicates despair, one of symptoms of depression. The change of tryptophan hydroxylase (TPH) in the dorsal raphe was investigated using immunohistochemistry. In the hippocampus cornu ammonis (CA) 1 and 3, glucocorticoid receptor (GR) expression was measured.Results: The immobility time in the FST was significantly lower (p < .05) in the low-dose (M = 32.40 ± 13.41 seconds) and middle-dose (M = 28.48 ± 19.57 seconds) groups than in the non-treated depressive rats (M = 90.19 ± 45.34 seconds). The amount of TPH in the dorsal raphe was significantly higher (p < .05) in the middle-dose (M = 249.17 ± 35.02) and high-dose (M = 251.0 ± 56.85) groups than in the non-treated depressive rats (M = 159.78 ± 41.16). However, GR expression in the hippocampus CA1 and CA3 did not show significant differences between the non-treated depressive rats and the capsaicin-injected rats.Conclusion: This study suggests that capsaicin produces an antidepressant-like effect on chronic unpredictable mild stress-induced depression in rats via the serotonin biosynthesis pathway.

The modified accelerated diagnostic protocol (ADP) to assess patients with chest pain symptoms using troponin as the only biomarker (mADAPT), the History, ECG, Age, Risk factors, and Troponin (HEART) pathway, and the Emergency Department Assessment of Chest Pain Rule (EDACS)-ADP, are the three most well-known ADPs for patients with chest pain. These ADPs define major adverse cardiac event (MACE) as components of acute myocardial infarction, revascularization, and death; unstable angina is not included as an endpoint.We performed a single-center prospective observational study comparing the performance of these 3 ADPs for patients with 30-day MACE with and without unstable angina. We hypothesized that these ADPs will have high sensitivities for MACE without unstable angina, a definition used for score derivation studies. However, when unstable angina is included in the MACE, their performances would be lower than the acceptable rate of99% sensitivity.A total of 1,214 patients were included in the analysis. When unstable angina was not included in the endpoint, sensitivities for MACE were 99.1% (95% confidence interval [CI]: 96.7-99.9%), 99.5% (95% CI: 97.4-100%), and 100% (95% CI: 98.3-100%) for mADAPT, EDACS-ADP, and HEART pathway, respectively. The HEART pathway had the highest proportion of patients classified as low risk (39.2%, 95% CI: 35.8-42.9%), followed by EDACS-ADP (31.3%, 95% CI: 28.2-34.6%) and mADAPT (29.3%, 95% CI: 26.4-32.5%). However, when unstable angina was included in the MACE, sensitivities were 96.6% (95% CI: 94.4-98.1%) for mADAPT, 97.3% (95% CI: 95.3-98.6%) for EDACS-ADP, and 97.3% (95% CI: 95.3-98.6%) for the HEART pathway, respectively. There were 15 false-negative cases with mADAPT, and 12 false-negative cases each for EDACS-ADP and HEART pathway.All three ADPs-mADAPT, EDACS-ADP, and HEART pathway-were similarly accurate in their discriminatory performance for the risk stratification of ED patients presenting with possible ACS when unstable angina was not included in the endpoint. The HEART pathway showed the best combination of sensitivity and proportion of patients that can be classified as safe for early discharge. However, when unstable angina was added to the endpoint, all three ADPs did not show appropriate safety levels and their performances were lower than the acceptable risk of MACE.

Objective Clinical trials on demodynamic-directed cardiopulmonary resuscitation have been limited. The aim of this study is to investigate whether Augmented-Medication CardioPulmonary Resuscitation (AMCPR) would improve the odds of return of spontaneous circulation (ROSC) in patients with out-of-hospital cardiac arrest.Methods This is a double-blind, single-center, randomized placebo-controlled trial that will be conducted in the emergency department of a tertiary, university-affiliated hospital in Seoul, Korea. A total of 148 adult patients with nontraumatic, nonshockable, out-of-hospital cardiac arrest who have an initial diastolic blood pressure above 20 mmHg will be randomly assigned to two groups of 74 patients (a 1:1 ratio). Patients will receive an intravenous dose of 40 IU of vasopressin with epinephrine, or a placebo with epinephrine. The primary endpoint is a sustained ROSC (over 20 minutes). Secondary endpoints are enhanced diastolic blood pressure, end-tidal carbon dioxide levels, acidosis, and lactate levels during resuscitation.Discussion AMCPR is a trial about tailored medication for select patients during resuscitation. This is the first randomized control trial to identify patients who would benefit from vasopressin for achieving ROSC. This study will provide evidence about the effect of administration of vasopressin with epinephrine to increase ROSC rate.Trial registration ClinicalTrials.gov identifier: NCT03191240. Registered on June 19, 2017.

Vascular aging is well known to be associated with the breakdown of the neurovascular unit (NVU), which is essential for maintaining brain homeostasis and linked to higher cognitive dysfunction. Oxidative stress is believed to be a significant cause of the vascular aging process. Vitamin C is easily oxidized under physiological conditions, so it loses its potent antioxidant activity. We developed a DNA aptamer that enhances the function of vitamin C. NXP032 is the binding form of the aptamer and vitamin C. In this study, we investigated the effect of NXP032 on neurovascular stabilization through the changes of PECAM-1, PDGFR-β, ZO-1, laminin, and glial cells involved in maintaining the integrity of the blood–brain barrier (BBB) in aged mice. NXP032 was orally administered daily for 8 weeks. Compared to young mice and NXP032-treated mice, 20-month-old mice displayed cognitive impairments in Y-maze and passive avoidance tests. NXP032 treatment contributed to reducing the BBB damage by attenuating the fragmentation of microvessels and reducing PDGFR-β, ZO-1, and laminin expression, thereby mitigating astrocytes and microglia activation during normal aging. Based on the results, we suggest that NXP032 reduces vascular aging and may be a novel intervention for aging-induced cognitive impairment.

This study determined the incidence of the cognitive impairments and mood disorders by telephone-based evaluation using previously mentioned scoring systems in out-of-hospital cardiac arrest (OHCA) survival with good neurologic outcome. Retrospective, cross-sectional, single-center study was performed, and a total of 97 patients were analyzed. Telephone version of Montreal Cognitive Assessment, Alzheimer’s disease-8 were used for evaluating cognitive dysfunctions, and the Patient Health Questionnaire-9 and the Hospital Anxiety and Depression Scale were used for assessing mood disorders. Quality of life was measured with the European Quality of Life 5-Dimension 5-Levels questionnaire. About one fourth patients experienced cognitive impairments (n = 23, 23.7%) or mood disorders (n = 28, 28.9%). Combined mood disorders (adjusted OR 21.36, 95% CI 5.14–88.84) and hospital length of stay (adjusted OR 1.04, 95% CI 1.01–1.08) were independent risk factors. In case of mood disorders, combined cognitive impairments (adjusted OR 9.94, 95% CI 2.83–35.97) and non-cardiac cause of cardiac arrest (adjusted OR 11.51, 95% CI 3.15–42.15) were risk factors. Furthermore, the quality of life was significantly low in the group with both cognitive impairments and mood disorders. Cognitive impairments and mood disorders were common among patients with good neurologic recovery.

Amelogenesis imperfecta (AI) is a heterogeneous collection of hereditary enamel defects. The affected enamel can be classified as hypoplastic, hypomaturation, or hypocalcified in form. A better understanding of normal amelogenesis and improvements in our ability to diagnose AI through genetic testing can be realized through more complete knowledge of the genes and disease-causing variants that cause AI. In this study, mutational analysis was performed with whole exome sequencing (WES) to identify genetic etiology underlying the hypomaturation AI condition in affected families. Mutational analyses identified biallelic WDR72 mutations in four hypomaturation AI families. Novel mutations include a homozygous deletion and insertion mutation (NM_182758.4: c.2680_2699delinsACTATAGTT, p.(Ser894Thrfs*15)), compound heterozygous mutations (paternal c.2332dupA, p.(Met778Asnfs*4)) and (maternal c.1287_1289del, p.(Ile430del)) and a homozygous 3694 bp deletion that includes exon 14 (NG_017034.2:g.96472_100165del). A homozygous recurrent mutation variant (c.1467_1468delAT, p.(Val491Aspfs*8)) was also identified. Current ideas on WDR72 structure and function are discussed. These cases expand the mutational spectrum of WDR72 mutations causing hypomaturation AI and improve the possibility of genetic testing to accurately diagnose AI caused by WDR72 defects.

We investigated the association between vitamin D deficiency and neurologic outcomes after cardiopulmonary resuscitation.Data from the prospective cardiac arrest registry in the emergency department between October 2019 and April 2021 were retrospectively analyzed. Blood samples were obtained during cardiopulmonary resuscitation wherein 25-hydroxyvitamin D serum levels were analyzed; deficiency was defined as levels 10 ng/mL. The primary outcome was neurologic outcomes at 3 months assessed using the modified Rankin Scale.A total of 195 patients (mean age, 64.5 ± 16.1 years; 135 [69.2%] men) were included. A significantly greater proportion of patients with poor outcomes had vitamin D deficiency compared with those with good outcomes (49.4% vs. 18.2%, P = 0.001). The area under the curve for a sustained return of spontaneous circulation and 3-month poor neurologic outcomes was 0.595 (P = 0.031) and 0.704 (P 0.001), respectively. In a multivariate analysis, vitamin D deficiency (odds ratio [OR]: 10.22; 95% confidence interval [CI]: 1.47-70.82, P = 0.019), initial shockable rhythm (OR: 0.03; 95% CI: 0.00-0.84, P = 0.040), low flow time (OR: 1.10; 95% CI: 1.03-1.16, P = 0.003), and thrombocytopenia (OR: 10.66; 95% CI: 1.13-100.41, P = 0.039) were significantly associated with 3-month poor neurologic outcomes.The prevalence of vitamin D deficiency in patients with cardiac arrest was 44% and was associated with poor neurological outcomes at 3 months.

Vascular aging is well known to be associated with breakdown of the neurovascular unit (NVU) that is essential for maintaining brain homeostasis and has been linked to higher cognitive dysfunction. Oxidative stress is believed to be a major cause of the vascular aging process, and damages cerebral parenchymal cells in aged brain. Vitamin C is easily oxidized under human physiologic conditions and loses its potent antioxidant activity. To overcome this limitation, we have developed a DNA aptamer that enhances function of vitamin C; NXP032 is binding form of Aptamer and vitamin C. We investigated microvascular damage, blood-brain barrier (BBB) disruption, glial activation, and cognitive function in 20-month-old mice to confirm the protective effect of NXP032 on vascular aging. NXP032 was treated orally for 8 weeks every day. In this study, we found that aged mice showed obvious cognitive impairment through Y-maze and passive avoidance tests. The microvascular damage was manifested through the decreased length of PECAM-1, lectin. BBB disruption was confirmed through the expression of PDGFR-β, ZO-1 and laminin. Aged mice also showed activation of microglia and astrocytes in the motor cortex and hippocampal CA1 region. These changes were significantly alleviated after the NXP032 treatment in aged mice. Based on the results, we suggest that the NXP032 reduces vascular aging which may be a novel intervention for aging-induced cognitive impairment.

Background The aim of this study was to evaluate prognostic value of body tissue composition at the upper thigh level for 1 year mortality in elderly patients with proximal femur fracture. Methods This retrospective cohort study included consecutive elderly (aged ≥65) patients diagnosed with proximal femur fracture based on the findings of pelvic bone computed tomography (CT) performed at the emergency department of a tertiary care hospital and treated with surgery between 2010 and 2017. The cross‐sectional area of subcutaneous fat and skeletal muscle at the upper thigh level was measured using CT. Adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for 1 year mortality were estimated using a Cox proportional hazards model. Survival based on the SFA quartiles was assessed using nonparametric Kaplan–Meier survival analysis and compared used log‐rank tests. Results Among 876 elderly patients included in this study, the median age was 79.0 years, and 646 (73.7%) patients were female. A total of 93 (10.6%) died within 1 year after admission to the emergency department. Survivors had a significantly higher median subcutaneous fat area (SFA) than non‐survivors (170.2 vs. 133.0 cm2, P 195.0 cm2) quartiles showed significantly longer survival duration than those with SFA in the first (

Chronic cerebral hypoperfusion (CCH) is caused by reduced blood flow to the brain representing gradually cognitive impairment. CCH induces mitochondrial dysfunction and neuronal cell death in the brain. Exercise is known to have a neuroprotective effect on brain damage and cognitive dysfunction. This study aimed to clarify the neuroprotective effect of low-intensity treadmill exercise (LITE) by enhancing cerebellar mitochondrial calcium retention capacity in an animal model of CCH. Wistar rats were divided into the sham group, the bilateral common carotid arteries occlusion (BCCAO) group, and the BCCAO and treadmill exercise (BCCAO+Ex) group. BCCAO+Ex group engaged the LITE on a treadmill for 30 min once a day for 8 weeks before the BCCAO surgery to investigate the protective effect of LITE on cognitive impairment. CCH induced by BCCAO resulted in mitochondrial dysfunction in the cerebellum, including impaired calcium homeostasis. CCH also decreased cerebellar Purkinje cells including of calbindin D28k and parvalbumin, resulting in cognitive impairment. The impairment of mitochondrial function, loss of cerebellar Purkinje cells, and cognitive dysfunction ameliorated by exercise. The present study showed that LITE hindered the deficit of spatial working memory and loss of Purkinje cell in the cerebellum induced by CCH. We confirmed that the protective effect of LITE on Purkinje cell by enhanced the mitochondrial calcium retention capacity. We suggest that LITE may protect against cognitive impairment, and further studies are needed to develop the intervention for patients who suffered from CCH.

OBJECTIVES We investigated awakening time and characteristics of awakening compared nonawakening and factors contributing to poor neurologic outcomes in out-of-hospital cardiac arrest survivors in no withdrawal of life-sustaining therapy settings. DESIGN Retrospective analysis of the Korean Hypothermia Network Pro registry. SETTING Multicenter ICU. PATIENTS Adult (≥ 18 yr) comatose out-of-hospital cardiac arrest survivors who underwent targeted temperature management at 33-36°C between October 2015 and December 2018. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS We measured the time from the end of rewarming to awakening, defined as a total Glasgow Coma Scale score greater than or equal to 9 or Glasgow Coma Scale motor score equals to 6. The primary outcome was awakening time. The secondary outcome was 6-month neurologic outcomes (poor outcome: Cerebral Performance Category 3-5). Among 1,145 out-of-hospital cardiac arrest survivors, 477 patients (41.7%) regained consciousness 30 hours (6-71 hr) later, and 116 patients (24.3%) awakened late (72 hr after the end of rewarming). Young age, witnessed arrest, shockable rhythm, cardiac etiology, shorter time to return of spontaneous circulation, lower serum lactate level, absence of seizures, and multisedative requirement were associated with awakening. Of the 477 who woke up, 74 (15.5%) had poor neurologic outcomes. Older age, liver cirrhosis, nonshockable rhythm, noncardiac etiology, a higher Sequential Organ Failure Assessment score, and higher serum lactate levels were associated with poor neurologic outcomes. Late awakeners were more common in the poor than in the good neurologic outcome group (38/74 [51.4%] vs 78/403 [19.4%]; p < 0.001). The awakening time (odds ratio, 1.005; 95% CIs, 1.003-1.008) and late awakening (odds ratio, 3.194; 95% CIs, 1.776-5.746) were independently associated with poor neurologic outcomes. CONCLUSIONS Late awakening after out-of-hospital cardiac arrest was common in no withdrawal of life-sustaining therapy settings and the probability of awakening decreased over time.

Disseminated intravascular coagulation (DIC) is a life-threatening complication of septic shock; however, risk factors for its development after admission are unknown. Thromboelastography (TEG) can reflect coagulation disturbances in early non-overt DIC that are not detected by standard coagulation tests. This study investigated the risk factors including TEG findings as early predictors for DIC development after admission in septic shock patients with non-overt DIC.This retrospective observation study included 295 consecutive septic shock patients with non-overt DIC at admission between January 2016 and December 2019. DIC was defined as an International Society on Thrombosis and Hemostasis (ISTH) score ≥ 5. The primary outcome was non-overt DIC at admission that met the ISTH DIC criteria within 3 days after admission.Of the 295 patients with non-overt DIC, 89 (30.2%) developed DIC after admission. The DIC group showed a higher ISTH score and 28-day mortality rate than the non-DIC group (2 vs. 3, P 0.001; 13.6% vs. 27.0%, P = 0.008, respectively). The DIC rate increased with the ISTH score (7.7%, 13.3%, 15.8%, 36.5%, and 61.4% for scores of 0, 1, 2, 3, and 4, respectively). Among TEG values, the maximum amplitude (MA) was higher in the non-DIC group (P 0.001). On multivariate analysis, an MA 64 mm was independently associated with DIC development (odds ratio, 2.311; 95% confidence interval, 1.298-4.115).DIC more often developed among those with admission ISTH scores ≥ 3 and was associated with higher mortality rates. An MA 64 mm was independently associated with DIC development in septic shock patients.

Background Previously conducted physician-centered trials on the usefulness of vasopressin have yielded negative results; thus, patient-oriented trials have been warranted. We hypothesize that Augmented-Medication CardioPulmonary Resuscitation could be helpful for selected patients with out-of-hospital cardiac arrest (OHCA). Methods This is a double-blind, single-center, randomized, placebo-controlled trial conducted in the emergency department in a tertiary, university-affiliated hospital in Seoul, Korea. A total of 148 adults with non-traumatic OHCA who had initial diastolic blood pressure (DBP) Results Of the 180 included patients, 32 were excluded, and 148 were enrolled in the trial. A sustained return of spontaneous circulation was achieved by 27 patients (36.5%) in the vasopressin group and 24 patients (32.4%) in the control group (risk difference, 4.1%; P = .60). Survival discharge and good neurologic outcomes did not differ between groups. The trial group had significantly higher median DBPs during resuscitation than the control group (16.0 vs. 14.5 mm Hg, P Conclusion Among patients with refractory vasodilatory shock in OHCA, administration of vasopressin, compared with placebo, did not significantly increase the likelihood of return of spontaneous circulation.

Background: Sepsis-related acute kidney injury is associated not only with short-term adverse effects but also important long-term consequences. However, differences and results across cancer patients remain unknown. Considering recent advances in both cancer and sepsis management, we were to evaluate the associated factors for occurrence of septic AKI and to determine the impact of septic acute kidney injury on the long-term mortality in cancer patients using a nationwide population-based cohort data with prohibited withdrawal of life-sustaining therapy.Methods: Using data from the National Health Insurance Service of Korea, adult cancer patients who presented to emergency department with septic shock from 2009 to 2017 were analyzed. Cox-proportional hazard model was conducted to evaluate the clinical effect of sepsis-related acute kidney injury requiring dialysis on the 2-year mortality.Results: Among 42,477 adult cancer patients with septic shock (90% solid and 10% hematologic cancer cases), dialysis-requiring acute kidney injury occurred in 5449 (12.8%) admission. Recovery from dialysis within 30-day was 77.9% and overall, 30-day and 2-year mortality rates were 52.1% and 85.1%, respectively. Oncologic patients with dialysis-requiring acute kidney injury were frequently occurred in male, history of hypertension, diabetes, congestive heart failure, liver cirrhosis, and patients with hematologic cancer. In multivariate Cox-proportional hazard model showed that dialysis-requiring acute kidney injury had a highest adjusted hazard ratio of 1.5 (95% confidence interval 31.31–1.40) for 2-year mortality.Conclusion: Dialysis-requiring septic acute kidney injury is not occurred commonly (about 13%). However, it had a significant association with the increased long-term mortality which emphasis on the prevention of acute kidney injury particularly in male hematologic cancer patients with comorbidities among the oncologic population.

The process of tooth formation is a series of reciprocal interactions between the ectoderm and mesoderm, and it is believed that many genetic factors are involved in this complex process. More than a dozen genes have been identified in non-syndromic tooth agenesis; however, the genetic etiology underlying tooth agenesis is not fully understood yet. In this study, we identified two novel LRP6 mutations in two non-syndromic oligodontia families. Both probands had 16 and 17 missing teeth in their permanent dentition. Mutational analysis identified a de novo frameshift mutation by a 1-bp insertion in exon 9 (NM_002336.2: c.1870dupA, p.(Met624Asnfs*29)) and a splicing donor site mutation in intron 8 (c.1762+2T>C). An in vitro splicing assay confirmed the deletion of exon 8, and the deletion would result in a frameshift. Due to the premature termination codons introduced by the frameshift, both mutant transcripts would be degraded by nonsense-mediated mRNA decay, resulting in haploinsufficiency.

The process of tooth formation is a series of reciprocal interactions between the ectoderm and mesoderm, and it is believed that many genetic factors are involved in this complex process. More than a dozen genes have been identified in non-syndromic tooth agenesis; however, the genetic etiology underlying tooth agenesis is not fully understood yet. In this study, we identified two novel

Purpose: This study aimed to evaluate the prognostic potential of muscle-related parameters (MRPs) at the level of the third lumbar vertebra (L3) using computerized tomography (CT) images in patients with stage I-III gastric cancer (GC) who underwent curative gastric resection. Methods: Patients with stage I-III GC who underwent curative gastric resection between October 2006 and June 2014 were enrolled in this study. In addition to demographic and clinical parameters, MRPs, such as skeletal muscle index (SMI), skeletal muscle radiation attenuation (SMRA), paraspinal muscle index (PMI), and paraspinal muscle radiation attenuation (PMRA), at the L3 level using CT images were collected and analyzed. The Kaplan-Meier method was used to estimate survival, and a Cox proportional hazard model was used to calculate the hazard ratio. In addition, the Pearson correlation coefficient was obtained as a measure of the linear relationship between the variables. Results: Data from 339 patients (233 men and 116 women) were analyzed. A strong correlation between SMI and PMI (r = 0.91); and SMRA and PMRA (r = 0.80) were observed, but only weak correlations between SMI and SMRA; and PMI and PMRA were found. When using the Cox model, SMRA or PMRA was a determinant of survival, but SMI and PMI were not. In the full model formed by adding SMRA or PMRA to a baseline model that included demographic and clinical variables, the C-index increased above 0.8, indicating excellent discrimination for both overall survival (OS) and disease-free survival (DFS). Moreover, the C-index of the model containing PMRA was higher than that of the model containing SMRA. Finally, there was a weak correlation between the prognostic nutritional index and SMRA or PMRA. Conclusions: With the multivariate Cox model, SMRA and PMRA appeared to determine survival. In addition, adding SMRA or PMRA to the baseline model increased the C-index above 0.8, indicating excellent discrimination for both OS and DFS. Moreover, compared to SMRA, the model containing PMRA appears to be a more accurate model for survival determination.

We investigated whether combining the pre-arrest serum albumin level could improve the performance of the Good Outcome Following Attempted Resuscitation (GO-FAR) score for predicting neurologic outcomes in in-hospital cardiac arrest patients. Adult patients who were admitted to a tertiary care hospital between 2013 and 2017 were assessed. Their pre-arrest serum albumin levels were measured within 24 h before the cardiac arrest. According to albumin levels, the patients were divided into quartiles and were assigned 1, 0, 0, and, − 2 points. Patients were allocated to the derivation (n = 419) and validation (n = 444) cohorts. The proportion of favorable outcome increased in a stepwise manner across increasing quartiles (p for trend p = 0.033). The results were consistent in the validation cohort (AUROC 0.799 vs. 0.791; p = 0.034). Net reclassification indices of the albumin-added model were 0.059 (95% confidence interval [CI] − 0.037 to 0.094) and 0.072 (95% CI 0.013–0.132) in the derivation and validation cohorts, respectively. An improvement in predictive performance was found by adding the ordinal scale of pre-arrest albumin levels to the original GO-FAR score.