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Outcomes of pediatric hepatoblastoma (HBL) have improved, but refractory cases still occur. More effective and safer drugs are needed that are based on molecular mechanisms. A disintegrin and metalloproteases (ADAMs) are expressed with high frequency in various human carcinomas and play an important role in cancer progression. In this study, we analyzed expression of ADAMs in HBL with a cDNA microarray dataset and found that the expression level of ADAM32 is particularly high. To investigate the role of ADAM32 in cancer, forced expression or knockdown experiments were conducted with HepG2 and HBL primary cells. Colony formation, cell migration and invasion, and cell viability were increased in HepG2 expressing ADAM32, whereas knockdown of ADAM32 induced a decrease in these cellular functions. Quantitative RT-PCR demonstrated an association between ADAM32 expression and the expression of genes related to cancer stem cells and epithelial–mesenchymal transition (EMT), suggesting a role of ADAM32 in cancer stemness and EMT. Furthermore, knockdown of ADAM32 increased cisplatin-induced apoptosis, and this effect was attenuated by a caspase-8 inhibitor, suggesting that ADAM32 plays a role in extrinsic apoptosis signaling. We conclude that ADAM32 plays a crucial role in progression of HBL, so it might be a promising molecular target in anticancer therapy.

We previously demonstrated that expression of a Krüppel-like zinc finger transcription factor, GLIS1, dramatically increases under hypoxic conditions via a transcriptional mechanism induced by HIF-2α cooperating with AP-1 members. In this study, we focused on the functional roles of GLIS1 in breast cancer. To uncover its biological function, the effects of altered levels of GLIS1 in breast cancer cell lines on cellular growth, wound-healing and invasion capacities were assessed. Knockdown of GLIS1 using siRNA in BT-474 cells resulted in significant growth stimulation under normoxia, while attenuation was found in the cell invasion assay under hypoxic conditions. In MDA-MB-231 cells expressing exogenous 3xFLAG-tagged GLIS1, GLIS1 attenuated cell proliferation and enhanced cell mobility and invasion capacities under normoxia. In addition, breast cancer cells expressing GLIS1 acquired resistance to irradiation. Whole transcriptome analysis clearly demonstrated that downstream signals of GLIS1 are related to various cellular functions. Among the genes with increased expression, we focused on WNT5A. Knockdown of WNT5A indicated that enhancement of acquired cell motility in the MDA-MB-231 cells expressing GLIS1 was mediated, at least in part, by WNT5A. In an analysis of publicly available data, patients with estrogen receptor-negative breast cancer showing high levels of GLIS1 expression showed much worse prognosis than those with low levels. In summary, hypoxia-induced GLIS1 plays significant roles in breast cancer cells via regulation of gene expression related to cell migration and invasion capacities, resulting in poorer prognosis in patients with advanced breast cancer.

Since understanding molecular mechanisms of SARS-CoV-2 infection is extremely important for developing effective therapies against COVID-19, we focused on the internalization mechanism of SARS-CoV-2 via ACE2. Although cigarette smoke is generally believed to be harmful to the pathogenesis of COVID-19, cigarette smoke extract (CSE) treatments were surprisingly found to suppress the expression of ACE2 in HepG2 cells. We thus tried to clarify the mechanism of CSE effects on expression of ACE2 in mammalian cells. Because RNA-seq analysis suggested that suppressive effects on ACE2 might be inversely correlated with induction of the genes regulated by aryl hydrocarbon receptor (AHR), the AHR agonists 6-formylindolo(3,2-b)carbazole (FICZ) and omeprazole (OMP) were tested to assess whether those treatments affected ACE2 expression. Both FICZ and OMP clearly suppressed ACE2 expression in a dose-dependent manner along with inducing CYP1A1. Knock-down experiments indicated a reduction of ACE2 by FICZ treatment in an AHR-dependent manner. Finally, treatments of AHR agonists inhibited SARS-CoV-2 infection into Vero E6 cells as determined with immunoblotting analyses detecting SARS-CoV-2 specific nucleocapsid protein. We here demonstrate that treatment with AHR agonists, including FICZ, and OMP, decreases expression of ACE2 via AHR activation, resulting in suppression of SARS-CoV-2 infection in mammalian cells.

Since understanding molecular mechanisms of SARS-CoV-2 infection is extremely important for developing effective therapies against COVID-19, we focused on the internalization mechanism of SARS-CoV-2 via ACE2. Although cigarette smoke is generally believed to be harmful to the pathogenesis of COVID-19, cigarette smoke extract (CSE) treatments were surprisingly found to suppress the expression of ACE2 in HepG2 cells. We thus tried to clarify the mechanism of CSE effects on expression of ACE2 in mammalian cells. Because RNA-seq analysis suggested that suppressive effects on ACE2 might be inversely correlated with induction of the genes regulated by aryl hydrocarbon receptor (AHR), the AHR agonists 6-formylindolo(3,2-b)carbazole (FICZ) and omeprazole (OMP) were tested to assess whether those treatments affected ACE2 expression. Both FICZ and OMP clearly suppressed ACE2 expression in a dose-dependent manner along with inducing CYP1A1. Knock-down experiments indicated a reduction of ACE2 by FICZ treatment in an AHR-dependent manner. Finally, treatments of AHR agonists inhibited SARS-CoV-2 infection into Vero E6 cells as determined with immunoblotting analyses detecting SARS-CoV-2 specific nucleocapsid protein. We here demonstrate that treatment with AHR agonists, including CSE, FICZ, and OMP, decreases expression of ACE2 via AHR activation, resulting in suppression of SARS-CoV-2 infection in mammalian cells.

Immunoparalysis is a common cause of death for critical care patients with sepsis, during which comprehensive suppression of innate and adaptive immunity plays a significant pathophysiological role. Although the underlying mechanisms are unknown, damage-associated molecular patterns (DAMPs) from septic tissues might be involved. Therefore, we surveyed sera from septic patients for factors that suppress the innate immune response to DAMPs, including adenosine triphosphate (ATP), monosodium urate, and high mobility group box-1. Macrophages, derived from THP-1 human acute monocytic leukemia cells, were incubated with each DAMP, in the presence or absence of sera that were collected from critically ill patients. Secreted cytokines were then quantified, and cell lysates were assayed for relevant intracellular signaling mediators. Sera from septic patients who ultimately did not survive significantly suppressed IL-1β production only in response to extracellular ATP. This effect was most pronounced with sera collected on day 3, and persisted with sera collected on day 7. However, this effect was not observed when THP-1 cells were treated with sera from survivors of sepsis. Septic sera collected at the time of admission (day 1) also diminished intracellular levels of inositol 1,4,5-triphosphate and cytosolic calcium (P < 0.01), both of which are essential for ATP signaling. Finally, activated caspase-1 was significantly diminished in cells exposed to sera collected on day 7 (P < 0.05). In conclusion, the sera of septic patients contain certain factors that persistently suppress the immune response to extracellular ATP, thereby leading to adverse clinical outcomes.

Although the biological systems in the human body are affected by the earth's gravity, information about the underlying molecular mechanisms is limited. For example, apoptotic signaling is enhanced in cancer cells subjected to microgravity. We reasoned that signaling regulated by p53 may be involved because of its role in apoptosis. Therefore, we aimed to clarify the molecular mechanisms of modified cis-diamminedichloroplatinum (CDDP)-sensitivity under simulated microgravity by focusing on p53-related cell death mechanisms. Immunoblotting analyses indicated that, under microgravity, CDDP-induced ATM/p53 signaling increased and caspase-3 was cleaved earlier. However, microgravity decreased the levels of expression of p53 targets BAX and CDKN1A. Interestingly, microgravity increased the PTEN, DRAM1, and PRKAA1 mRNA levels. However, microgravity decreased the levels of mTOR and increased the LC3-II/I ratio, suggesting the activation of autophagy. The CDDP-induced cleavage of caspase-3 was increased during the early phase in Group MG (+), and cleaved caspase-3 was detected even in Group MG (+) with constitutive expression of a mutant type of p53 (hereafter, "+" indicates CDDP treatment). These results interestingly indicate that microgravity altered CDDP sensitivity through activation of caspase-3 by p53-independent mechanism.

Tumor hypoxia contributes to a biologically aggressive phenotype and therapeutic resistance. Recent studies have revealed that hypoxia reduces expression of several DNA damage recognition and repair (DRR) genes via both hypoxia-inducible factor (HIF)-independent and -dependent pathways, and this induced genomic instability in cancer cells. We show here that one of the HIF-target genes—differentiated embryo chondrocyte (DEC)—plays a role in DNA damage response via transcriptional repression. Comprehensive gene expression and database analyses have revealed systemic repression of DNA-DRR genes in cancer and non-cancer cells under hypoxic conditions. Hypoxic repression in typical cases was confirmed by quantitative RT-PCR and promoter reporter experiments, and knockdown experiments indicated the critical role of DEC2 in such repression. Assessment of histone H2AX phosphorylation revealed that recognition and repair of DNA double-strand breaks (DSBs) induced by bleomycin or γ-ray irradiation were attenuated; moreover, Cleaved Caspase-3 levels were decreased with pre-conditioning under hypoxia: opposing phenomena were ascertained by knockdown of DEC2. Finally, pre-conditioning under hypoxia decreased the sensitivity of cancer cells to DSBs, and knockdown of DEC2 increased γ-ray sensitivity. These data imply that a critical reduction of DNA-DRR occurs via DEC-dependent transcriptional repression and suggest that DEC is a potential molecular target for anti-cancer strategies.

Summary 437 nuclear power plants are in operation at present around the world to meet increasing energy demands. Unfortunately, five major nuclear accidents have occurred in the past—ie, at Kyshtym (Russia [then USSR], 1957), Windscale Piles (UK, 1957), Three Mile Island (USA, 1979), Chernobyl (Ukraine [then USSR], 1986), and Fukushima (Japan, 2011). The effects of these accidents on individuals and societies are diverse and enduring. Accumulated evidence about radiation health effects on atomic bomb survivors and other radiation-exposed people has formed the basis for national and international regulations about radiation protection. However, past experiences suggest that common issues were not necessarily physical health problems directly attributable to radiation exposure, but rather psychological and social effects. Additionally, evacuation and long-term displacement created severe health-care problems for the most vulnerable people, such as hospital inpatients and elderly people.

Backgrounds: Japanese patients with idiopathic pulmonary fibrosis (IPF) appear to experience acute exacerbation (AE-IPF) more frequently than other ethnicities. Aims: To investigate pathogenetic gene polymorphisms in developing AE-IPF. Methods: A total of 139 patients with IPF (86 German and 53 Japanese) were enrolled. The correlation between ethnicity, polymorphisms in potential pathogenetic genes ( MUC1, MUC5B, ELMOD2, HER2, IL8, TERT, Caveolin, EGF, HMOX1, ICAM1, VEGFA, DPP9, ATP11A, OBFC1, DSP, FAM13A1, TOLLIP) and the incidence of AE-IPF was evaluated. Results: Six (7%) German and 17 (32%) Japanese patients experienced AE-IPF during the first 3 years of follow-up. In the univariate analysis, Japanese ethnicity, lower vital capacity, non-use of triple therapy (prednisone, azathioprine and N-acetylcysteine), the polymorphisms in MUC1, TERT, DPP9 and ATP11A gene were risk factors for AE-IPF. In the multivariate analysis, A/A polymorphisms in TERT gene and A/A polymorphisms in MUC1 gene were independent risk factors for AE-IPF (HR=53.6, p=0.0089; HR=8.2, p=0.042, respectively). The C statistic for TERT and MUC1 gene polymorphisms in addition to covariates including Japanese ethnicity was 0.896 (p TERT and MUC1 gene polymorphisms in addition to covariates was 0.914 (p Conclusions: TERT and MUC1 gene polymorphisms appear to be risk factors for AE-IPF.

A 50-year-old construction worker had been pressed down beneath a forklift truck and sustained cardiopulmonary arrest. Physical findings were typical for traumatic asphyxia. The patient was resuscitated by a bystander using only external cardiac compression; rescue breathing was not performed. He had both coma and cardiopulmonary arrest persisted for 7 min until emergency medical technicians (EMT) arrived. However, he was resuscitated in cooperation with bystander, EMT, a nearest hospital and our hospital on resuscitation. Nearly full recovery ultimately resulted. Even incomplete resuscitation performed immediately by a bystander may offer a better chance of survival and permit a better functional outcome in traumatic asphyxia than proficient but delayed cardiopulmonary resuscitation.

Direct hemoperfusion with polymyxin B-immobilized fiber (PMX-DHP) might be beneficial for treating acute exacerbation (AE) of interstitial pneumonia (IP). Venovenous extracorporeal membranous oxygenation (VV-ECMO) is an emerging tool to avoid ventilator-induced lung injury. This is a report presenting the first three patients with AE of IP treated with a combined therapy of PMX-DHP and VV-ECMO.Patient 1 was a 68-year-old male with acute interstitial pneumonia, patient 2 a 67-year-old male with AE of idiopathic pulmonary fibrosis, and patient 3 a 61-year-old female with AE of collagen vascular disease-associated interstitial pneumonia. All patients were severely hypoxemic and required mechanical ventilation. A combined therapy using PMX-DHP and VV-ECMO was initiated with support of intravenous corticosteroids and antibiotics. Radiological findings, oxygenation and laboratory findings markedly improved and all patients survived without severe complications.A combined therapy of PMX-DHP and VV-ECMO might be a therapeutic option for AE of IP.

We sought to establish the clinical utility of the Pentax-AWS Airway Scope(®) (AWS) when used by paramedics to intubate the trachea, and to evaluate whether their performance was influenced by previous clinical experience with the Macintosh laryngoscope (ML).Twenty paramedics attempted tracheal intubation using the AWS in five patients each in the operating room. We recorded the success rate, the number of intubation attempts, and the time for intubation and adverse events, and compared these based on the paramedics' previous clinical experience with the ML. Ten paramedics had no prior clinical experience of the ML (group A) and 10 had used it on more than 30 occasions (group B).The intubation success rate was 99 % (99/100). Notably, 96 % (47/49) of intubations were achieved on the first attempt by the inexperienced paramedics in group A, compared with 64 % (32/50) by the experienced paramedics in group B (p = 0.0001). The time to intubation (mean ± SD) was significantly shorter in group A than in group B (37 ± 24 vs. 48 ± 21 s, p = 0.002). There were marked variations in the times taken to intubate, but no apparent improvement as the intubators gained experience between their first and fifth cases. No complications were encountered in either group.We found that paramedics could achieve a high tracheal intubation success rate using the AWS independent of previous airway management experience. Better intubation performance with the AWS was observed in paramedics without clinical experience with the ML.

Yasumasa Iwasaki1, Akira Namera2, Hiroshi Giga1, Yoshiko Kida1, Kohei Ota1, Kazunobu Une1, Tadatsugu Otani1, Shinichiro Ohshimo1, Nobuyuki Hirohashi1, Koichi Tanigawa1 1Department of Emergency and Critical Care Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan 2Department of Forensic Medicine, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan *Corresponding author: Yasumasa Iwasaki, Department of Emergency and Critical Care Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan, Tel: 81-90-8242-4859; E-mail: yiwasaki@hiroshima-u.ac.jp

Many studies have established that pretreatment of mouse macrophages with LPS will alter subsequent responsiveness of these cells to stimulation either with LPS or other stimuli. Incubation of C3Heb/FeJ mouse macrophages with low sub-stimulatory (e.g. 0.10 ng/ml) LPS for 6 h, followed by activation with 100 ng/ml of LPS results in up-regulation of LPS-dependent TNFα production and suppression of the ability of these cells to secrete nitric oxide (NO). To assess whether these two responses might be co-ordinately regulated, immunocytochemical analyses of LPS-pretreated macrophages were carried out using anti-TNFα and anti-iNOS antibodies, both with and without a period of LPS pretreatment. As anticipated, the detection of individual iNOS-expressing macrophages in LPS-stimulated cultures accurately reflected threshold doses of LPS required for detection of NO in culture supernatants in terms of frequency of percentage of the total population positive for expression of iNOS protein. Pretreatment with sub-stimulatory doses of LPS significantly reduced the frequency of these iNOS-expressing macrophages responsive to subsequent LPS stimulation, supporting the concept of iNOS down-regulation at the pretranslational level. In contrast, the detection of TNFα-expressing macrophages in LPS-stimulated cultures did not correlate directly with the detection of TNFα in culture supernatants. Further, pretreatment with sub-stimulatory doses of LPS did not always correlate with the frequency of TNFα-expressing cells in response to LPS treatment. These results support the concept that different regulatory mechanisms may be operative in differential regulation of macrophage TNFα and NO responsiveness by pretreatment of macrophages with sub-stimulatory doses of LPS.

The Airway scope® (AWS), the KingVision® (KV) and the McGRATH® (MG) are new indirect video laryngoscopes designed to facilitate effective and safe tracheal intubation under various conditions. However, there are few comparative studies as for performance in tracheal intubation attempted by inexperienced personnel. The purpose of this study was to evaluate success rates, time to intubation with use of these devices by inexperienced personnel in a simulated manikin difficult airway.

Background: Venoarterial-venous extracorporeal membrane oxygenation (VAV ECMO) configuration is a combined procedure of extracorporeal membrane oxygenation (ECMO). The proportion of cardiac and respiratory support can be controlled by adjusting arterial and venous return. Therefore, VAV ECMO can be applicable as a bridging therapy in the transition from venoarterial (VA) to venovenous (VV) ECMO. Case presentation: We present an 11-year-old girl with chemotherapy-induced myocarditis requiring extracorporeal cardiorespiratory support. She showed progressive hypotension, tachycardia, hyperlactemia, and tachypnea under support of catecholamines. Echocardiography showed severe left ventricular hypokinesis with an ejection fraction of 30 %. She was placed on VA ECMO with a drainage catheter from the right femoral vein (19.5 Fr) and a return catheter to the right femoral artery (16.5 Fr). Extracorporeal circulation was initiated at a blood flow of 2.0 L/min (59 mL/kg/min). On day 31, although cardiac function had improved, persistent pulmonary failure made weaning from VA ECMO difficult. We planned transition from VA ECMO to VAV ECMO to ensure gradual tapering of extracorporeal cardiac support while evaluating cardiopulmonary function. An additional return cannula (13.5 Fr) was inserted from the right internal jugular vein, which was connected to the circuit branch from the original returning cannula. We then gradually shifted the blood from the femoral artery to the right internal jugular vein over 24 h. She was successfully switched from VA to VV ECMO via VAV ECMO. Conclusions: VAV ECMO might be an option in ensuring oxygenation to the coronary circulation and allowing time to adequately evaluate cardiac function during transition from VA to VV ECMO. Further investigations using larger cohorts are necessary to validate the efficacy of VAV ECMO as a bridging therapy in the transition from VA to VV ECMO., This work was supported by a JSPS KAKENHI Grant (Number JP 16K09541).

Background KL-6 is a mucin-like glycoprotein expressed on the surface of alveolar type II cells. Elevated concentrations of KL-6 in serum and epithelial lining fluid (ELF) in patients with acute respiratory distress syndrome (ARDS) have been previously reported; however, kinetics and prognostic significance of KL-6 have not been extensively studied. This study was conducted to clarify these points in ARDS patients. Methods Thirty-two patients with ARDS who received mechanical ventilation under intubation were studied for 28 days. ELF and blood were obtained from each patient at multiple time points after the diagnosis of ARDS. ELF was collected using a bronchoscopic microsampling procedure, and ELF and serum KL-6 concentrations were measured. Results KL-6 levels in ELF on days 0 to 3 after ARDS diagnosis were significantly higher in nonsurvivors than in survivors, and thereafter, there was no difference in concentrations between the two groups. Serum KL-6 levels did not show statistically significant differences between nonsurvivors and survivors at any time point. When the highest KL-6 levels in ELF and serum sample from each patient were examined, KL-6 levels in both ELF and serum were significantly higher in nonsurvivors than in survivors. The optimal cut-off values were set at 3453 U/mL for ELF and 530 U/mL for serum by receiver operating characteristic (ROC) curve analyses. Patients with KL-6 concentrations in ELF higher than 3453 U/mL or serum concentrations higher than 530 U/mL had significantly lower survival rates up to 90 days after ARDS diagnosis. Conclusions ELF and serum KL-6 concentrations were found to be good indicators of clinical outcome in ARDS patients. Particularly, KL-6 levels in ELF measured during the early period after the diagnosis were useful for predicting prognosis in ARDS patients.

Although bystander cardiopulmonary resuscitation (CPR) can improve survival from cardiac arrest, the reported prevalence of bystander CPR remains low in most countries. This study was performed to investigate factors affecting laypersons' willingness in performing CPR.

The Airway Scope (AWS) (Pentax-AWS, Hoya Corp., Tokyo, Japan) and the Airtraq (ATQ) (Prodol, Vizcaya, Spain) have similarities in the novel structures of their blades. In this study, we evaluated the ease of use of the AWS and ATQ compared with the Macintosh laryngoscope (ML) by inexperienced personnel in a simulated manikin difficult airway.Twenty-four fifth-year medical students with no previous experience in tracheal intubation participated in this study. We used an advanced patient simulator (SimMan(R), Laerdal Medical, Stavanger, Norway) to simulate difficult airway scenarios including cervical spine rigidity, limited mouth opening, and pharyngeal obstruction. The sequences in selecting devices and scenarios were randomized. Success rates for tracheal intubation, and the time required for visualization of the glottis, tracheal intubation, and inflation of the lungs, and the number of optimization maneuvers and dental click sounds were analyzed. The 3 different intubation devices were tested in 4 different scenarios by 24 students.Both the AWS and ATQ had very high success rates of tracheal intubation compared with the ML (AWS 100%*; ATQ 98%*; and ML 89%; *P0.05 AWS, ATQ versus ML). The time to intubation with the AWS was significantly shorter than with the ATQ and ML (AWS 11 +/- 6 seconds; ATQ 16 +/- 12 seconds; and ML 16 +/- 11 seconds; *P0.05 AWS versus ATQ, ML). The number of optimization maneuvers with the AWS was significantly lower than with the ATQ and ML. There were significantly more audible dental click sounds with the ML than with the AWS and ATQ.Both the AWS and ATQ may be suitable devices for difficult intubation by inexperienced personnel in this manikin simulated scenario. Further studies in a clinical setting are necessary to confirm these findings.

Airway pressure release ventilation (APRV) is a ventilatory mode that allows unsupported spontaneous breathing at any phase of the ventilatory cycle with high mean airway pressures. We hypothesized that use of APRV might produce potential beneficial effects on oxygenation, reducing mortality in patients with severe acute respiratory distress syndrome (ARDS) in comparison with synchronized intermittent mandatory ventilation (SIMV) as a conventional mode of ventilation. We retrospectively reviewed data of 58 patients with severe ARDS (the ratios of partial arterial oxygen tension to fraction of inspired oxygen, PaO2/F(I)O2 ratio150). The patients' data were divided into two groups: SIMV-group and APRV-group. Patients' backgrounds, oxygenation on day 0, 1, 3, 5 and 7 following initiation of each mode, vasopressor dependence, duration of ventilation, duration of ICU stay, and mortality in ICU were analyzed. PaO2/F(I)O2 ratios were statistically higher in the APRV-group (APRV vs. SIMV on day 1, 3, 5, 7: 201.6 +/- 76 vs.150 +/- 59.1, 256.7 +/- 71.5 vs.182.1 +/- 65.4, 268.8 +/- 73.3 vs. 204.6 +/- 72.8, and 263 +/- 74.5 vs. 204.1 +/- 67.1, respectively, p0.05). Vasopressors were less used (p=0.018), and mortality in ICU tended to be lower in the APRV group (31%) than in the SIMV group (59%) (p=0.050). Use of APRV in patients with severe ARDS appears to be associated with improvements in oxygenation, and a trend toward lower mortality in ICU. No significant adverse effects were observed. Prospective controlled studies are required to confirm the benefits of this ventilatory mode in comparison with conventional methods for severe ARDS.

The Airway Scope (AWS-S100, Pentax, Tokyo, Japan) is a new video-laryngoscope, which has a specially designed blade and a portable, battery-powered, 2.4-inch built-in liquid crystal device (LCD) full-color video screen at the top of the handle. In this study, we tested the usefulness of the AWS for tracheal intubation in acute, urgent situations. Patients admitted to the Advanced Emergency and Critical Care Center at Hiroshima University Hospital and who required orotracheal intubations were prospectively enrolled. Tracheal intubations were performed using the AWS by residents (the novice group) or staff physicians (the experienced group), who received a brief instruction in the AWS. We enrolled 38 patients (23 males, 15 females; age, 60 +/- 19 years). Intubations were attempted by 22 intubators (11 residents and 11 experienced personnel). The durations from inserting the blade via the oral cavity until observing the glottis (T1), inserting the tube into the trachea (T2), and confirming the chest rise (T3) were 22 +/- 15, 34 +/- 21 and 49 +/- 27 sec, respectively. When the results were classified into t experienced and novice groups, T1, T2 and T3 were 17 +/- 10 vs. 26 +/- 17, 32 +/- 23 vs. 36 +/- 20, and 45 +/- 25 vs. 53 +/- 27 sec, respectively (the experienced vs. the novice group, n.s.). These results suggested that the AWS may be a suitable device particularly for less experienced personnel, such as novice Advanced Life Support providers.

High quality of chest compressions during cardiopulmonary resuscitation (CPR) is a critical determinant of outcome from out-of-hospital cardiac arrest (OHCA). Unfortunately, however, victims often do not receive adequate chest compression for various reasons, particularly during transportation. Recent studies have demonstrated the interruption time of chest compression using transthoracic impedance analysis, but more information is needed to evaluate the performance of CPR provided by ambulance crews and reveal reasons for hands off chest during CPR.

Venovenous extracorporeal membrane oxygenation (VV ECMO) is a treatment option for acute respiratory distress syndrome (ARDS) to minimize ventilator-induced lung injury including life- threatening pneumothorax. The purpose of our study was to investigate the safety and efficacy of VV ECMO for preventing pneumothorax in ARDS patients who were complicated with emphysematous/cystic changes in the lung.

Methicillin-resistant Staphylococcus aureus (MRSA) is a leading pathogen of hospital-acquired pneumonia. The difference in outcome between patients with imported and newly-isolated MRSA in the ICU has not been well investigated. The aim of our study was to explore the incidence, risk factors and outcome in patients with imported and newly-isolated MRSA.

Surface molecules involved in human T cell activation were investigated using a newly developed monoclonal antibody (H47 mAb). H47 antigen (Ag) recognized by H47 mAb was expressed on approximately 10% of resting T cells (mostly CD4-CD8+), 30% of phorbol 12-myristate 13-acetate (PMA)-activated T cells (both CD4+CD8- and CD4-CD8+), and most NK, B cells, and monocytes in the peripheral blood mononuclear cells (PBMC). H47 mAb respectively immunoprecipitated a 100 or 120-kD molecular weight (MW) membrane protein of T cells and monocytes under nonreducing or reducing conditions, suggesting that H47 Ag consists of a single polypeptide that has intramolecular disulfide bonds. H47 mAb significantly enhanced PMA-induced proliferation of PBMC in a monocyte-independent fashion. H47 mAb, however, failed to enhance T cell proliferation induced by anti-CD3 mAb, anti-CD2 mAb, or phytohemagglutinin (PHA). H47 mAb also enhanced PMA-induced interleukin-2 receptor (IL-2R) expression and IL-2 synthesis, but did not induce a change in intracellular free calcium ([Ca2+]i) of T cells. These results suggest that H47 Ag is a new membrane molecule involved in PMA-induced T cell activation.

We developed and characterized a monoclonal antibody (mAb), H227, recognizing a new epitope of human 4F2 molecular complex whose roles remain to be identified. Both staining patterns and molecular sizes recognized by H227 mAb were the same to those of 4F2 mAb. Thus, both H227 and 4F2 mAbs were reactive to monocytes, thymocytes, and activated lymphocytes and immunoprecipitated the 125-kDa molecular weight membrane protein under nonreducing conditions and 85-kDa heavy-chain and 40-kDa light-chain proteins under reducing conditions. These two mAbs immunoprecipitated only the 85-kDa heavy-chain protein when the cell lysate was initially treated with dithiothreitol. Sequential immunoprecipitation proved their cross-reactivity. Both the mAbs inhibited phytohemagglutinin- or concanavalin A-induced proliferation of peripheral blood mononuclear cells (PBMC). In contrast to these similarities, the pretreatment of cells with one mAb failed to block the reactivity to the other, suggesting that their epitopes were different from each other. Furthermore, only H227 mAb augmented phorbol myrislate acetate (PMA)-induced PBMC proliferation in association with increase in interleukin 2 receptor expression. In summary, H227 mAb recognizes a new epitope of 4F2 heavy chain that might be involved in the PMA-induced T cell activation pathway and therefore shall be a useful tool for understanding the roles of the 4F2 molecular complex.