Takeshi Yagi

Serum Glial Fibrillary Acidic Protein Is a Highly Specific Biomarker for Traumatic Brain Injury in Humans Compared With S-100B and Neuron-Specific Enolase

BACKGROUND Serum glial fibrillary acidic protein (GFAP) is a specific predictor of brain damage and neurologic outcome in patients with traumatic brain injury (TBI). In this study, serum GFAP, S-100B, and neuron-specific enolase (NSE) were compared in the same samples from severe trauma patients to assess their ability to predict abnormalities detectable on head computed tomography (CT). METHODS This study was a retrospective analysis at a single university emergency center. Thirty-four trauma patients were included. Serum samples were collected from the patients for 3 days. Serum GFAP, S-100B, and NSE concentrations were measured with enzyme-linked immunosorbent assays and compared in patients with and without TBI, as evaluated by head CT. RESULTS Serum GFAP, S-100B, and NSE were significantly higher in the TBI patients than in the non-TBI patients (p < 0.05 for each protein). The receiver operating characteristic curves for TBI were compared for the three biomarkers for 3 days. Serum GFAP on day 1 had the largest area under the receiver operating characteristic curve (0.983), with 88.9% sensitivity and 100% specificity. CONCLUSIONS Serum GFAP has remarkable diagnostic value for TBI, defined by abnormal head CT findings, in prehospital-triaged patients with severe trauma.

Urinary trypsin inhibitor suppresses excessive superoxide anion radical generation in blood, oxidative stress, early inflammation, and endothelial injury in forebrain ischemia/reperfusion rats.

Abstract Objectives: To investigate the effects of ulinastatin, a urinary trypsin inhibitor (UTI), on jugular venous superoxide radical (O−2·) generation, oxidative stress, early inflammation, and endothelial activation in forebrain ischemia/reperfusion (FBI/R) rats.Methods: Fourteen Wistar rats were allocated to a control group (n = 7) and a UTI group (n = 7). Throughout the experiments, O−2· in the jugular vein was measured by the produced current using a novel electrochemical O−2· sensor. Forebrain ischemia was induced by occlusion of the bilateral common caroti darteries with hemorrhagic hypotension for 20 min, followed by reperfusion. In the UTI group, UTI (5 U/g) was administered intravenously immediately after reperfusion. At 60 min after reperfusion, plasma and brain were harvested, and malondialdehyde, high-mobility group box 1 (HMGB1) protein, and intercellular adhesion molecule-1 (ICAM-1) were measured. Results: O−2· current increased gradually during forebrain ischemia in both groups. The current increased markedly in the control group immediately after reperfusion but was significantly attenuated in the UTI group after reperfusion. Brain and plasma malondialdehyde, HMGB1, and ICAM-1 were significantly attenuated in the UTI group compared with those in the control group, except for brain HMGB1, which was associated with the amount of O−2· generated during FBI/R. Discussion: UTI suppressed jugular venous O−2· generation, oxidative stress, early inflammation, and endothelial activation in FBI/R rats. Therefore, UTI might be a useful agent for the therapy of the cerebral ischemia/reperfusion pathophysiology.

Effects of mechanical chest compression device with a load-distributing band on post-resuscitation injuries identified by post-mortem computed tomography.

OBJECTIVE To determine the effects of cardiopulmonary resuscitation (CPR) with AutoPulse™ (LDB-CPR) on post-resuscitation injuries identified by post-mortem computed tomography (PMCT). AutoPulse™ is a novel mechanical chest-compression device with a load-distributing band (LDB) that may affect post-resuscitation injury identified by PMCT. METHODS We conducted a retrospective cohort study of non-traumatic adult out-of-hospital cardiac arrest patients whose death was confirmed in our emergency department between October 2009 and September 2014. Patients were divided according to whether LDB-CPR (LDB-CPR group) or manual CPR only (manual CPR only group) was performed. The background characteristics and post-resuscitation injuries identified by PMCT were compared between both groups. Logistic regression was used to identify risk factors for posterior rib fracture and abdominal injury. RESULTS Overall, 323 patients were evaluated, with 241 (74.6%) in the LDB-CPR group. The total duration of CPR was significantly longer in the LDB-CPR group than in the manual CPR only group. Posterior rib fracture, hemoperitoneum, and retroperitoneal hemorrhage were significantly more frequent in the LDB-CPR group. The frequencies of anterior/lateral rib and sternum fracture were similar in both groups. Pneumothorax tended to be more frequent in the LDB-CPR group, although not significantly. LDB-CPR was an independent risk factor for posterior rib fracture (odds ratio 30.57, 95% confidence interval 4.15-225.49, P=0.001) and abdominal injury (odds ratio 4.93, 95% confidence interval 1.88-12.95, P=0.001). CONCLUSIONS LDB-CPR was associated with higher frequencies of posterior rib fracture and abdominal injury identified by PMCT. PMCT findings should be carefully examined after LDB-CPR.

Cholinergic agonist physostigmine suppresses excessive superoxide anion radical generation in blood, oxidative stress, early inflammation, and endothelial injury in rats with forebrain ischemia/reperfusion.

The cholinergic anti-inflammatory pathway is reportedly important in modulating the inflammatory response in local and systemic diseases, including ischemia/reperfusion pathophysiology. In this study, we investigated the effects of the cholinergic agonist, physostigmine, on jugular venous superoxide radical (O(2)(-)) generation, oxidative stress, early inflammation, and endothelial activation during forebrain ischemia/reperfusion (FBI/R) in rats. Fourteen male Wistar rat were allocated to the control group (n=7) or physostigmine group (n=7). The physostigmine group received 80 ng/g physostigmine intraperitoneally 24 h and 1 h before forebrain ischemia was established. The jugular venous O(2)(-) current was measured for 10 min during forebrain ischemia and for 120 min after reperfusion. The O(2)(-) current increased gradually during forebrain ischemia in both groups. The current increased markedly immediately after reperfusion in the control group but was significantly attenuated in the physostigmine group after reperfusion. Brain and plasma malondialdehyde, high-mobility group box 1 (HMGB1) protein, and intercellular adhesion molecule 1 (ICAM1) were significantly attenuated in the physostigmine group compared with the control group, except for brain HMGB1. The amount of O(2)(-) generated during FBI/R correlated with malondialdehyde, HMGB1, and ICAM1 in both the brain and plasma. In conclusion, the cholinergic agonist physostigmine suppressed jugular venous O(2)(-) generation, oxidative stress, early inflammation, and endothelial activation in the brain and plasma in the acute phase of cerebral ischemia/reperfusion. Therefore, the suppression of O(2)(-) is a key mechanism of the cholinergic anti-inflammatory pathway in the pathophysiology of cerebral ischemia/reperfusion.

Moderate hypothermia suppressed excessive generation of superoxide anion radical and inflammatory reactions in blood and liver in heatstroke: Laboratory study in rats

Abstract The study was performed to demonstrate superoxide radical (O2·–) generation, systemic inflammation and liver injury caused by heatstroke and to reveal suppressive effects of moderate hypothermia. Heatstroke was defined as achieving pharyngeal temperature of 40°C with arterial pressure reduction. Heatstroke rats were divided to four groups by the temperature after the onset; 40°C, 37°C, 32°C and sham-treated with 37°C. O2·– current was measured continuously in the right atrium using an electrochemical O2·– senor. The O2·– current increased in all groups except for the sham-treated group during the induction. After the onset of heatstroke, the O2·– current was suppressed with temperature-dependency. Plasma and liver high-mobility group box 1, intercellular adhesion molecule-1, plasma aspartate aminotransferase and alanine aminotransferase were also suppressed with the suppression of O2·– generation. Therefore, excessive O2·– generation might be a key factor in heatstroke and the suppression with moderate hypothermia would be a therapeutic modality.

Staged Surgical Repair for Extensive Cardiovascular Damage by Syphilis

A 45-year-old man had aortic regurgitation with a syphilitic true aneurysm of the ascending to transverse arch aorta and a descending aortic aneurysm from chronic Stanford type B aortic dissection. After antibiotic therapy, two-staged surgical repair was performed and there has been no evidence of recurrence in 12 months since the second stage. We describe the successful management of extensive cardiovascular syphilitic damage.

Global end-diastolic volume, serum osmolarity, and albumin are risk factors for increased extravascular lung water

BACKGROUND The transpulmonary thermodilution technique allows the determination of cardiac preload (global end-diastolic volume index) and quantification of pulmonary edema (extravascular lung water index [EVLWI]). Pulmonary edema commonly develops in critically ill patients; however, the underlying pathophysiology, that is, hydrostatic (cardiac) or permeability-induced (noncardiac), often remains unclear. In this study, hemodynamic and serum parameters of osmolarity and oncotic pressure were analyzed to identify risk factors for increased EVLWI. METHODS A retrospective, single-center analysis in an intensive care unit of a university hospital was performed. No interventions were made for the study. Forty-two critically ill patients were included, and 126 simultaneous hemodynamic measurements and serum determinations were analyzed by logistic regression and Spearman rank correlation coefficient analysis. RESULTS Global end-diastolic volume index (P = .001), serum albumin (P = .006), and serum osmolarity (P = .029) were significant factors for increased EVLWI (defined as >10 mL/kg). CONCLUSION Hypervolemia, hypoalbuminemia, and high plasma osmolarity are associated with increased EVLWI.

Mitral valve repair in patient with absent right superior vena cava in visceroatrial situs solitus

We report on a 74-year-old woman with an absence of right superior vena cava in visceroatrial situs solitus who underwent mitral valve plasty for severe mitral regurgitation. Preoperative three-dimensional computed tomography revealed an absent right and persistent left superior vena cava that drained into the right atrium by way of the coronary sinus. Perioperaively, placement of pulmonary artery catheter, site of venous cannulation, and management of associated rhythm abnormalities were great concern. Obtaining the information about this central venous malformation preoperatively, we performed mitral valve plasty without any difficulties related to this anomaly.

Early enteral nutrition is associated with reduced in-hospital mortality from sepsis in patients with sarcopenia

Purpose: To determine whether the association of early enteral nutrition (EEN) with mortality from sepsis differs between patients with and without sarcopenia. Materials and methods: We retrospectively reviewed septic patients treated at our centre between January 2010 and August 2017. The skeletal muscle area (SMA) at the level of the third lumbar vertebra was measured with CT on admission, and sarcopenia was defined as SMA < 80% of the predicted value. Patients were divided into two subgroups (sarcopenic and non‐sarcopenic patients), and in‐hospital mortality was compared in patients treated with and without EEN within each subgroup. We used logistic regression to examine factors associated with in‐hospital mortality in each subgroup. Results: EEN was administered to 35/91 sarcopenic patients and 43/100 non‐sarcopenic patients. In‐hospital mortality did not differ between non‐sarcopenic patients with EEN and those without EEN (16% vs 16%, P = 0.947), but was significantly lower in sarcopenic patients with EEN than in those without EEN (9% vs 34%, P = 0.005). Logistic regression showed that EEN was independently associated with reduced in‐hospital mortality in sarcopenic patients (OR 0.18, 95% CI 0.05–0.71, P = 0.014), but not in non‐sarcopenic patients. Conclusions: EEN may be more beneficial in sarcopenic patients. HighlightsEffects of early enteral nutrition (EEN) on mortality from sepsis remain uncertain.Effects of EEN may differ with patient characteristics.EEN was independently associated with reduced in‐hospital mortality in sarcopenia, but not in non‐sarcopenia.Sarcopenic patients may be a suitable sub‐group for EEN.

Splenic volume in severe sepsis is associated with disease severity and pneumococcal infection

A small spleen, which is occasionally found in patients with pneumococcal sepsis, may increase pneumococcal susceptibility because of splenic malfunction. However, a small spleen may also originate from severe disease. We carried out a retrospective study to evaluate the association between splenic volume and severe pneumococcal sepsis or disease severity.