Electrospun Manganese-Based Metal-Organic Frameworks for MnOx Nanostructures Embedded in Carbon Nanofibers as a High-Performance Nonenzymatic Glucose Sensor.

Material-specific electrocatalytic activity and electrode design are essential factors in evaluating the performance of electrochemical sensors. Herein, the technique described involves electrospinning manganese-based metal-organic frameworks (Mn-MOFs) to develop MnOx nanostructures embedded in carbon nanofibers. The resulting structure features an electrocatalytic material for an enzyme-free glucose sensor. The elemental composition, morphology, and microstructure of the fabricated electrodes materials were characterized by using energy-dispersive X-ray spectroscopy (EDX), field-emission scanning electron microscopy (FESEM), and transmission electron microscopy (TEM). Cyclic voltammetry (CV) and amperometric i-t (current-time) techniques are characteristically employed to assess the electrochemical performance of materials. The MOF MnOx-CNFs nanostructures significantly improve detection performance for nonenzymatic amperometric glucose sensors, including a broad linear range (0 mM to 9.1 mM), high sensitivity (4080.6 µA mM-1 cm-2), a low detection limit (0.3 µM, S/N = 3), acceptable selectivity, outstanding reproducibility, and stability. The strategy of metal and metal oxide-integrated CNF nanostructures based on MOFs opens interesting possibilities for the development of high-performance electrochemical sensors.

In Vivo and In Vitro Biodistribution of Inulin-Tethered Boron-Doped Amine-Functionalized Carbon Dots.

Carbon dots (CDs) are considered a potential substance for use in biomarker applications due to their exceptional light stability. However, there are several unsolved uncertainties about CD toxicity in vitro and in vivo. In this study, a redesigned derivative of the natural polysaccharide inulin is connected with boron-doped amine-functionalized carbon dots (In@BN-CDs) through carbodiimide coupling to improve the biocompatibility of the nanoformulation. The toxicity and biodistribution of ln@BN-CDs in vivo and in vitro were explored in detail. The In@BN-CDs were tested after a single inhalation dosage of 10, 7, 5, 3, and 1 mg/kg. We explored a dose- and time-dependent technique of collecting blood samples and then centrifuged the blood samples and obtained serum samples, which were then analyzed for fluorescence inspection; findings showed that the fluorescence intensity decreased with time. Similarly, In@BN-CDs were effectively used as in vitro toxicity and fluorescent probes for cellular imaging in living cells due to their biocompatibility and cell membrane accessibility. The biocompatibility and efficacy of In@BN-CDs as fluorescent imaging agents have been demonstrated. The data suggest that the usage of In@BN-CDs in vitro and in vivo should be examined.

Emphysematous Salmonella-Infected Aneurysm of the Aortic Arch: Case Report.

BACKGROUND: Infected aortic aneurysm is a relatively rare disease with significant morbidity and mortality. Because of its deeper position, patients with infected aortic arch aneurysms may present with only fever and other vague symptoms, such as weakness, fatigue, dizziness, anorexia, and functional decline. It is difficult confirm a diagnosis that is based solely on history or physical examination, and it may only be apparent on imaging studies. CASE REPORT: We present a brief case report of a patient presenting to the emergency department with unexplained fever who was diagnosed with emphysematous salmonella-infected aneurysm of the aortic arch. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Infected aortic arch aneurysm is an extremely unusual disease entity that emergency physicians encounter. Because of the high mortality and morbidity of this catastrophic disease, an infected aortic aneurysm should be considered as a possible diagnosis in patients with persistent fever and vague symptoms without a specific infection focus. To avoid delayed diagnosis, emergency physicians should be aware of infected aortic arch aneurysm.

Suicide attempt using sodium nitrite ordered on the internet: Two case reports.

RATIONALE: Sodium nitrite is a potent oxidizing agent that impairs oxygen transport and delivery through methemoglobin formation. Clinical manifestations are known to induce methemoglobinemia, dysrhythmia, hypotension, and even death. While accidental intoxication of sodium nitrite by contaminated water and food has previously occurred, there has been a substantial upsurge in suicide intoxication in recent years. PATIENT CONCERNS: We present case reports of 2 patients who attempted suicide by sodium nitrite after ordering a "suicide powder" on the internet market. They were brought to the emergency department after attempting suicide by ingesting sodium nitrite. They experienced dyspnea, cyanosis, and mild nausea. DIAGNOSIS: Based on their history and blood tests, methemoglobinemia was initially diagnosed. INTERVENTIONS AND OUTCOMES: The patients received methylene blue antidotal therapy in the emergency department. The patients were discharged after neuropsychiatric evaluation and treatment for mental illness, suicidal ideation, and suicide attempts. They informed us of how simple and easy it was for them to buy sodium nitrite for suicidal purposes. LESSONS: With widely shared information on the usage of sodium nitrite for suicide and the absence of proper regulation, the incidence of acute poisoning will increase. This increases physicians' chances of encountering unexplained cyanosis and methemoglobinemia. Clinical suspicion of sodium nitrite intoxication is warranted in cases of unexplained cyanosis or methemoglobinemia. We want to highlight how simple and easy it is to buy sodium nitrite for suicidal purposes.

Prediction of Severe Injury in Bicycle Rider Accidents: A Multicenter Observational Study.

Introduction: This study aimed to establish a predictive model that includes physiological parameters and identify independent risk factors for severe injuries in bicycle rider accidents. Methods: This was a multicenter observational study. For four years, we included patients with bicycle rider injuries in the Emergency Department-Based Injury In-depth Surveillance database. In this study, we regarded ICD admission or in-hospital mortality as parameters of severe trauma. Univariate and multivariate logistic regression analyses were performed to assess risk factors for severe trauma. A receiver operating characteristic (ROC) curve was generated to evaluate the performance of the regression model. Results: This study included 19,842 patients, of whom 1,202 (6.05%) had severe trauma. In multivariate regression analysis, male sex, older age, alcohol use, motor vehicle opponent, load state (general and crosswalk), blood pressure, heart rate, respiratory rate, and Glasgow Coma Scale were the independent factors for predicting severe trauma. In the ROC analysis, the area under the ROC curve for predicting severe trauma was 0.848 (95% confidence interval: 0.830-0.867). Conclusion: We identified independent risk factors for severe trauma in bicycle rider accidents and believe that physiologic parameters contribute to enhancing prediction ability.

Effect of therapeutic hypothermia against renal injury in a rat model of asphyxial cardiac arrest: Α focus on the survival rate, pathophysiology and antioxidant enzymes.

Although multi­organ dysfunction is associated with the survival rate following cardiac arrest (CA), the majority of studies to date have focused on hearts and brains, and few studies have considered renal failure. The objective of the present study, therefore, was to examine the effects of therapeutic hypothermia on the survival rate, pathophysiology and antioxidant enzymes in rat kidneys following asphyxial CA. Rats were sacrificed one day following CA. The survival rate, which was estimated using Kaplan­Meier analysis, was 42.9% one day following CA. However, hypothermia, which was induced following CA, significantly increased the survival rate (71.4%). In normothermia rats with CA, the serum blood urea nitrogen level was significantly increased one day post­CA. In addition, the serum creatinine level was significantly increased one day post­CA. However, in CA rats exposed to hypothermia, the levels of urea nitrogen and creatinine significantly decreased following CA. Histochemical staining revealed a significant temporal increase in renal injury after the normothermia group was subjected to CA. However, renal injury was significantly decreased in the hypothermia group. Immunohistochemical analysis of the kidney revealed a significant decrease in antioxidant enzymes (copper­zinc superoxide dismutase, manganese superoxide dismutase, glutathione peroxidase and catalase) with time in the normothermia group. However, in the hypothermia group, these enzymes were significantly elevated following CA. Collectively, the results revealed that renal dysfunction following asphyxial CA was strongly associated with the early survival rate and therapeutic hypothermia reduced renal injury via effective antioxidant mechanisms.

Therapeutic hypothermia effect on asphyxial cardiac arrest-induced renal ischemia/reperfusion injury via change of Nrf2/HO-1 levels.

The present study aimed to investigate the renoprotective effect of therapeutic hypothermia (TH) on renal ischemia-reperfusion injury (RI/RI) induced by asphyxial cardiac arrest (CA) in rats. A total of 48 male rats were randomly divided into five groups: i) Sham (n=6); ii) Normothermia + CA (Normo.) (n=14); iii) Normo. and 2 h of TH after return of spontaneous circulation (ROSC) (n=12); iv) Normo. and 4 h of TH after ROSC (n=9); and v) Normo. and 6 h of TH after ROSC (n=7). All rats except the Sham group underwent asphyxia CA and were sacrificed 1 day after ROSC. The survival rate increased from 42.8% in the Normo. group to 50, 66.6 and 85.7% in the groups with 2, 4 and 6 h of TH after CA, respectively. TH attenuated the histopathological changes of the renal tissues following ROSC and the levels of blood urea nitrogen, serum creatinine and malondialdehyde in renal tissues. On immunohistochemistry, the relative optical density of nuclear erythroid-related factor-2 (Nrf2) and heme oxygenase (HO-1) expression in renal tissues increased in the Normo. group compared with that in the Sham group and exhibited further significant increases at 6 h of TH after ROSC. In conclusion, TH attenuated renal injury and increased the expression of Nrf2 and HO-1 in a TH treatment time-dependent manner.

Changes of renal histopathology and the role of Nrf2/HO-1 in asphyxial cardiac arrest model in rats.

PURPOSE: To investigate the role of Nrf2/HO-1 in renal histopathological ailments time-dependently in asphyxial cardiac arrest (CA) rat model. METHODS: Eighty-eight Sprague Dawley male rats were divided into five groups of eight rats each. Asphyxial CA was induced in all the experimental rats except for the sham group. The rats were sacrificed at 6 hours, 12 hours, one day and two days post-CA. Serum blood urea nitrogen (BUN), creatinine (Crtn) and malondialdehyde from the renal tissues were evaluated. Hematoxylin and eosin and periodic acid-Schiff staining were done to evaluate the renal histopathological changes in the renal cortex. Furthermore, Nrf2/HO-1 immunohistochemistry (ihc) and western blot analysis were performed after CA. RESULTS: The survival rate of rats decreased in a time-dependent manner: 66.6% at 6 hours, 50% at 12 hours, 38.1% in one day, and 25.8% in two days. BUN and serum Crtn markedly increased in CA-operated groups. Histopathological ailments of the renal cortical tissues increased significantly from 6 hours until two days post-CA. Furthermore, Nrf2/HO-1 expression level significantly increased at 6 hours, 12 hours, and one day. CONCLUSIONS: The survival rate decreased time-dependently, and Nrf/HO-1 expression increased from 6 hours with the peak times at 12 hours, and one day post-CA.

Changes of renal histopathology and the role of Nrf2/HO-1 in asphyxial cardiac arrest model in rats

ABSTRACT Purpose To investigate the role of Nrf2/HO-1 in renal histopathological ailments time-dependently in asphyxial cardiac arrest (CA) rat model. Methods Eighty-eight Sprague Dawley male rats were divided into five groups of eight rats each. Asphyxial CA was induced in all the experimental rats except for the sham group. The rats were sacrificed at 6 hours, 12 hours, one day and two days post-CA. Serum blood urea nitrogen (BUN), creatinine (Crtn) and malondialdehyde from the renal tissues were evaluated. Hematoxylin and eosin and periodic acid-Schiff staining were done to evaluate the renal histopathological changes in the renal cortex. Furthermore, Nrf2/HO-1 immunohistochemistry (ihc) and western blot analysis were performed after CA. Results The survival rate of rats decreased in a time-dependent manner: 66.6% at 6 hours, 50% at 12 hours, 38.1% in one day, and 25.8% in two days. BUN and serum Crtn markedly increased in CA-operated groups. Histopathological ailments of the renal cortical tissues increased significantly from 6 hours until two days post-CA. Furthermore, Nrf2/HO-1 expression level significantly increased at 6 hours, 12 hours, and one day. Conclusions The survival rate decreased time-dependently, and Nrf/HO-1 expression increased from 6 hours with the peak times at 12 hours, and one day post-CA.

Protective effects of therapeutic hypothermia on renal injury in an asphyxial cardiac arrest rat model.

Cardiac arrest (CA) is a leading cause of mortality worldwide. Most of post-resuscitation related deaths are due to post-cardiac arrest syndrome (PCAS). After cardiopulmonary resuscitation (CPR), return of spontaneous circulation (ROSC) leads to renal ischemia-reperfusion injury, also known as PCAS. Many studies have focused on brain and heart injuries after ROSC, but renal failure has largely been ignored. Therefore, we investigated the protective effects of therapeutic hypothermia (TH) on asphyxial CA-induced renal injury in rats. Thirty rats were randomly divided into five groups: 1) the control group (sham); 2) the normothermic CA (nor.); 3) a normothermic CA group that received TH immediately within 2 h after CPR (Hypo. 2 hrs); 4) a normothermic CA group that received TH within 4 h after CPR (Hypo. 4 hrs); and 5) a normothermia CA group that received TH within 6 h after CPR (Hypo. 6 h). One day after CPR, all rats were sacrificed. Compared with the normothermic CA group, the TH groups demonstrated significantly increased survival rate (P < 0.05); decreased serum blood urea nitrogen, creatinine, and lactate dehydrogenase levels; and lower histological damage degree and malondialdehyde concentration in their renal tissue. Terminal deoxynucleotidyl transferase dUTP nick end labeling stain revealed that the number of apoptotic cells significantly decreased after 4 h and 6 h of TH compared to the results seen in the normothermic CA group. Moreover, TH downregulated the expression of cyclooxygenase-2 in the renal cortex compared to the normothermic CA group one day after CPR. These results suggest that TH exerts anti-apoptotic, anti-inflammatory, and anti-oxidative effects immediately after ROSC that protect against renal injury.

Mortality difference between early-identified sepsis and late-identified sepsis.

OBJECTIVE: The aim of the study was to compare the mortality rates of patients with early-identified (EI) sepsis and late-identified (LI) sepsis. METHODS: We performed a retrospective chart review of patients admitted to the emergency department and diagnosed with sepsis. EI sepsis was defined as patients with a Sequential Organ Failure Assessment (SOFA) score ≥2, based on 3 parameters of the SOFA score (Glasgow coma scale, mean arterial pressure, and partial pressure of oxygen/fraction of inspired oxygen ratio), measured within an hour of emergency department admission. The remaining patients were defined as LI sepsis. The primary outcome was in-hospital mortality. RESULTS: Of the total 204 patients with sepsis, 113 (55.4%) had EI sepsis. Overall mortality rate was 15.7%, and EI sepsis group had significantly higher mortality than LI sepsis (23.0% vs. 6.6%, P=0.003). The patients with EI sepsis, compared to those with LI sepsis, had higher SOFA score (median: 4 vs. 2, P<0.001); Acute Physiology and Chronic Health Evaluation (APACHE) II score (median: 14 vs. 10, P<0.001); were more likely to progress to septic shock within 6 hours after admission (17.7% vs. 1.1%, P<0.001); were more likely to be admitted to the intensive care unit (2.2% vs. 1.1%, P=0.001). CONCLUSION: Mortality was significantly higher in the EI sepsis group than in the LI sepsis group.

Change in jaw occlusive power by paralysis of masseter muscle with a neuromuscular blocker: Sion's masseter muscle paralysis.

STUDY OBJECTIVE: We aimed to determine whether jaw occlusive power decreases with the injection of neuromuscular blocking agents in masseter muscle - a method we named Sion's masseter muscle paralysis (SMP). METHODS: A randomized, placebo-controlled animal study was conducted in which researchers were blinded to group allocation. We used 12 male mongrel dogs aged 10-12 months and weighing 30-35 kg. Four groups were formed: a conventional dose (CD) group (0.004 mg/kg succinylcholine in 4 ml normal saline [NS]); a high dose (HD) group (0.04 mg/kg succinylcholine in 4 ml NS); a placebo group (4 ml NS); and no intervention group. To measure the jaw occlusive power, 1 kg weight was hung sequentially on a specifically designed device on the animal's lower jaw. At -4, -2, 0', +2, +4, +6, +8, +10, +20, and +30 min, we measured the jaw occlusive power, oxygen saturation (SpO2), and end-tidal carbon dioxide (ETCO2). RESULTS: After SMP, jaw occlusive power began to decline in CD and HD group. The arithmetical mean jaw occlusive power values at -4, -2, 0', +2, +4, +6, +8, and +10 min were 9.7, 9.7, 9.7, 8.7, 8.3, 7.3, 6.7, and 6.3 kgw in the CD group and 9.7, 9.3, 8.7, 8.0, 6.7, 5.0, 5.0, and 5.3 kgw in the HD group. No abnormalities in SpO2or ETCO2were detected. CONCLUSION: Jaw occlusive power was decreased after SMP with succinylcholine, without inducing respiratory complication.

Factors for modifying the termination of resuscitation rule in out-of-hospital cardiac arrest.

BACKGROUND: False positive rate (FPR) of the current basic life support (BLS) termination of resuscitation (TOR) rule in out-of-hospital cardiac arrest (OHCA) patients (not witnessed; no return of spontaneous circulation prior to transport; and no shocks were delivered) has been ethically challenging. We validated the current BLS TOR rule with using nationwide Korean Cardiac Arrest Research Consortium (KoCARC) registry and identified the factors for modifying the rules. METHODS: This prospective, multicenter, registry-based study was performed using the nontraumatic OHCA registry data between October 2015 and June 2017. Independent factors associated with poor neurologic outcome were identified to propose new KoCARC TOR rules by using multivariable analysis. The diagnostic performances of the TOR rules were calculated respectively. RESULTS: Among 4,360 OHCA patients, 2,801 (64.2%) satisfied all 3 criteria of the BLS TOR rule. The FPR and positive predictive value of the BLS TOR rule were 5.9% and 99.3%. Asystole as initial rhythm and age > 60 years were found as new factors for modifying the TOR rule. New KoCARC TOR rules, combination of asystole and age > 60 years with current TOR rule, showed lower FPR (0.3%-2.1%) and higher positive predictive value (99.7%-99.9%) for predicting poor neurologic outcome at discharge. CONCLUSIONS: In this recent nationwide cohort, the current BLS TOR rule showed high FPR (5.9%) for predicting poor neurologic outcome. We anticipate that our new KoCARC TOR rules, application of 2 new factors (asystole as initial rhythm and age > 60 years) with BLS TOR rule, could reduce unwarranted death.

Serial evaluation of SOFA and APACHE II scores to predict neurologic outcomes of out-of-hospital cardiac arrest survivors with targeted temperature management.

OBJECTIVE: This study was aimed at a serial evaluation and comparison of the prognostic values of Sequential Organ Failure Assessment (SOFA) and Acute Physiology and Chronic Health Evaluation (APACHE) II scores for neurologic outcomes in comatose, out-of-hospital cardiac arrest (OHCA) survivors, treated with targeted temperature management (TTM). METHODS: We analysed a prospective cohort of comatose OHCA patients, with TTM, admitted to an emergency intensive care unit (ICU), between January 2010 and December 2015. SOFA and APACHE II scores were calculated initially, and then at day 1, 2, 3, 5, and 7 after ICU admission. Primary and secondary outcomes were the 28-day neurologic outcome and the 28-day mortality, respectively. Prognostic value of the SOFA and APACHE II scores was analysed using the receiver operating characteristic curve. RESULTS: Of the 143 selected patients, 62 survived and 34 had good neurologic outcomes at day 28. There was no significant difference in the SOFA and extracerebral SOFA scores between the good and poor neurologic outcome groups. However, the APACHE II scores were significantly higher in the good outcome group; they displayed good discriminatory power in predicting poor outcomes, unlike the SOFA scores. The APACHE II score at day 3 had the highest prognostic value for predicting poor neurologic outcomes with an area under the cure of 0.793, and with a cut-off value of 20, the APACHE II score predicted poor neurologic outcomes with a sensitivity of 43.75%, a specificity of 94.12%, a positive predictive value of 94.59%, and a negative predictive value of 41.56%. CONCLUSIONS: Identifying APACHE II score might assist as one piece of multimodal prognostic approach for the assessment of neurologic outcomes in OHCA survivors treated with TTM.