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• A total 21 quality indicators of palliative care were settled. • Symptom palliation and supporting decision-making process are two major domains. • Outcome measure could only be evaluated by bereaved family survey. Although recent attention to palliative care for patients with cardiovascular diseases has been increasing, there are no specific recommendations on detailed palliative care practices. We proceed on a discussion of the appropriateness and applicability of potential quality indicators for acute cardiovascular diseases according to our previous systematic review. We created a multidisciplinary panel of 20 team members and 7 external validation clinicians composed of clinical cardiologists, a nutritionist, a physiotherapist, a clinical psychologist, a critical and emergent care specialist, a catheterization specialist, a primary care specialist, a palliative care specialist, and nurses. After crafting potential indicators, we performed a Delphi rating, ranging from "1 = minimum" to "9 = maximum". The criterion for the adoption of candidate indicators was set at a total mean score of seven or more. Finally, we subcategorized these indicators into several domains by using exploratory factor analysis. Sixteen of the panel members (80%) were men (age, 49.5 ± 13.7 years old). Among the initial 32 indicators, consensus was initially reached on total 23 indicators (71.8%), which were then summarized into 21 measures by selecting relatively feasible time variations. The major domains were "symptom palliation" and "supporting the decision-making process". Factor analysis could not find optimal model. Narratively-developed seven sub-categories included "presence of palliative care team", "patient-family relationship", "multidisciplinary team approach", "policy of approaching patients", "symptom screening and management", "presence of ethical review board", "collecting and providing information for decision-maker", and "determination of treatment strategy and the sharing of the care team's decision". In this study we developed 21 quality indicators, which were categorized into 2 major domains and 7 sub-categories. These indicators might be useful for many healthcare providers in the initiation and enhancement of palliative care practices for acute cardiovascular diseases in Japan. [ABSTRACT FROM AUTHOR]

The Xenopus LIM homeodomain protein Xlim-1 is specifically expressed in the Spemann organizer region and assumed to play a role in the establishment of the body axis as a transcriptional activator. To further elucidate the mechanism underlying the regulation of its transcriptional activity, we focused on the region C-terminal to the homeodomain of Xlim-1 (CT239-403) and divided it into five regions, CCR1-5 (C-terminal conserved regions), based on similarity between Xlim-1 and its paralog, Xlim-5. The role of Xlim-1 CT239-403 in the Spemann organizer was analyzed by assaying the axis-forming ability of a series of CCR-mutated constructs in Xenopus embryos. We show that high doses of Xlim-1 constructs deleted of CCR1 or CCR2 initiate secondary axis formation in the absence of its coactivator Ldb1 (LIM-domain-binding protein 1), suggesting that CCR1 and CCR2 are involved in negative regulation of Xlim-1. In contrast, while Xlim-1 is capable of initiating secondary axis formation at low doses in the presence of Ldb1, deletion of CCR2 (aa 275-295) or substitution of five conserved tyrosines in CCR2 with alanines (CCR2-SYA) abolished the activity. In addition, UAS-GAL4 one-hybrid reporter assays in Xenopus showed that CCR2, but not CCR2-5YA, with its flanking regions (aa 261-315) functions as a transactivation domain when fused to the GAL4 DNA-binding domain. Finally, we show that none of the known transcriptional coactivators tested (CBP, SRC-1, and TIF2) interacts with the Xlim-1 transactivation domain (aa 261-315). Thus, Xlim-1 not only contains a unique tyrosine-rich activation domain but also contains a negative regulatory domain in CT239-403, suggesting a complex regulatory mechanism underlying the transcriptional activity of Xlim-1 in the organizer. [C] 2000 Academic Press Key Words: Xenopus laevis; Spemann organizer; axis formation; transcription factor; LIM homeodomain protein; LIM domain; negative regulation; transactivation; Xlim-1; Ldb1.

The homeobox genes Xlim-1 and goosecoid (gsc) are coexpressed in the Spemann organizer and later in the prechordal plate that acts as head organizer. Based on our previous finding that gsc is a possible target gene for Xlim-1, we studied the regulation of gsc transcription by Xlim-1 and other regulatory genes expressed at gastrula stages, by using gsc-luciferase reporter constructs injected into animal explants. A 492-bp upstream region of the gsc promoter responds to Xlim-1/3m, an activated form of Xlim-1, and to a combination of wild-type Xlim-1 and Ldb1, a LIM domain binding protein, supporting the view that gsc is a direct target of Xlim-1. Footprint and electrophoretic mobility shift assays with GST-homeodomain fusion proteins and embryo extracts overexpressing FLAG-tagged full-length proteins showed that the Xlim-1 homeodomain or Xlim-1/Ldb1 complex recognize several TAATXY core elements in the 492-bp upstream region, where XY is TA, TG, CA, or GG. Some of these elements are also bound by the ventral factor PV.1, whereas a TAATCT element did not bind Xlim-1 or PV.1 but did bind the anterior factors Otx2 and Gsc. These proteins modulate the activity of the gsc reporter in animal caps: Otx2 activates the reporter synergistically with Xlim-1 plus Ldbl, whereas Gsc and PV.1 strongly repress reporter activity. We show further, using animal cap assays, that the endogenous gsc gene was synergistically activated by Xlim-1, Ldb1, and Otx2 and that the endogenous otx2 gene was activated by Xlim-1/3m, and this activation was suppressed by the posterior factor Xbra. Based on these data, we propose a model for gene interactions in the specification of dorsoventral and anteroposterior differences in the mesoderm during gastrulation. [C] 2000 Academic Press Key Words: Xenopus; head organizer; homeobox gene; goosecoid promoter; Xlim-1; Ldb1; Otx2; Gsc; PV.1; Xvent-1; Xbra; LIM domain.

Background: The prevalence of anisakiasis is rare in the United States and Europe compared with that in Japan, with few reports of its presentation in the emergency department (ED). This study describes the clinical, hematologic, computed tomographic (CT) characteristics, and treatment in gastric and small intestinal anisakiasis patients in the ED. Methods: We retrospectively reviewed the data of 83 consecutive anisakiasis presentations in our ED between 2003 and 2012. Gastric anisakiasis was endoscopically diagnosed with the Anisakis polypide. Small intestinal anisakiasis was diagnosed based on both hematologic (Anisakis antibody) and CT findings. Results: Of the 83 cases, 39 had gastric anisakiasis and 44 had small intestinal anisakiasis based on our diagnostic criteria. Although all patients had abdominal pain, the gastric anisakiasis group developed symptoms significantly earlier (peaking within 6 hours) than the small intestinal anisakiasis group (peaking within 48 hours), and fewer patients with gastric anisakiasis needed admission therapy (5% vs 57%, P<.01). All patients in the gastric and 40 (91%) in the small intestinal anisakiasis group had a history of raw seafood ingestion. Computed tomographic findings revealed edematous wall thickening in all patients, and ascites and phlegmon of the mesenteric fat were more frequently observed in the small intestinal anisakiasis group. Conclusions: In the ED, early and accurate diagnosis of anisakiasis is important to treat and explain to the patient, and diagnosis can be facilitated by a history of raw seafood ingestion, evaluation of the time-to-symptom development, and classic CT findings. [ABSTRACT FROM AUTHOR]

Abstract: Aim: Therapeutic hypothermia (TH) is widely used as a cardioprotective treatment for cardiac arrest. TH at 30–32°C during ischaemia and reperfusion has a cardioprotective effect. The aims of the study were to examine whether TH at 34°C with late induction (immediately after the start of reperfusion) has a cardioprotective effect and to determine if this effect is mediated by nitric oxide (NO) and phosphatidylinositol 3′-kinase (PI3K). Methods: Langendorff perfusion of Sprague–Dawley rat hearts was initiated at 75mmHg at 37°C. Left ventricle infarct sizes were evaluated by triphenyltetrazolium chloride staining after Langendorff perfusion in 6 groups (each n =7): control group; ischaemia group, with 34°C TH during ischaemia for 30min and reperfusion for 180min; reperfusion group, with 34°C TH induced solely during the reperfusion period; the l-NAME (NO synthase inhibitor), LY294002, and wortmannin (PI3K inhibitors) groups, which were treated similarly to the reperfusion group with the addition of each compound. Results: TH reduced the left ventricle infarct size from 54.2±14.8% of the control group to 11.9±6.3% (ischaemia group, p <0.001) and to 23.5±10.5% (reperfusion group, p <0.001). l-NAME, LY294002, and wortmannin reversed the cardioprotective effect of TH induced during reperfusion to 42.5±10.6% (p =0.009), 40.9±4.1% (p =0.021), and 51.9±13.0% (p <0.001), respectively. Circulatory temperatures reached 34°C within 5min in all groups subjected to TH. Conclusions: TH of 34°C showed a cardioprotective effect even with late initiation of cooling during reperfusion. The effect was mediated by NO and PI3K. [Copyright &y& Elsevier]

Abstract: Background: Anion gap (AG) is a useful index for assessing the clinical condition of critically ill patients especially in intoxication. Recently, AG can be obtained easily using a blood gas analyzer (BGA); however, its reliability requires validation. Methods: We enrolled patients who simultaneously underwent blood gas analysis and blood test in the central hospital laboratory and patients who visited the emergency department of our hospital from January 1, 2004, to December 31, 2007. The deviation of AG calculated using the BGA and that calculated by the central hospital laboratory were extracted. From the data obtained using the BGA, the independent risk factor causing a significant error in AG was statistically analyzed. Results: A total of 2922 patients were enrolled, of which 339 were defined as the significant error group. Male sex, abnormal Hco 3 −, abnormal lactate, abnormal K, abnormal Cl, and abnormal Na were the independent risk factors producing the significant error. The results indicate that regardless of whether the original electrolyte data of the patients are abnormal, when the electrolyte measurement results obtained using the BGA are abnormal, the calculated AG might show a significant error. In addition, the fact that lactate was determined as a risk factor indicates that AG might be more useful in patients who have intoxication than in those under an unstable state in terms of vital signs. Conclusion: When risk factors are present, the medical condition of a patient should be reevaluated by comparing results without heavily relying on the AG obtained by a BGA. [Copyright &y& Elsevier]

Abstract: A large quantity of white gas containing titanium dioxide and hydrogen chloride was generated unexpectedly during an experiment in a chemical laboratory. Fourteen students and staff complained of nausea, dyspnea, or respiratory irritation immediately after inhaling the gas. On arrival at Saint Luke''s International Hospital, more than half of the patients presented with low-grade fever. Symptoms spontaneously resolved soon after admission, although the low-grade fever persisted until the following morning. Low-grade fever after inhalation exposure is not explicable by hydrogen chloride inhalation and therefore appeared to be caused by titanium dioxide inhalation, manifesting as metal fume fever. Titanium dioxide is thought to have no remarkable human toxicity and is considered to be safe clinically. To our knowledge, this is the first report of titanium dioxide inhalation as the potential cause of metal fume fever in humans. Correlations between the degree of fever and quantity and concentration of inhaled titanium dioxide remain to be determined. [Copyright &y& Elsevier]

Signals by cytokines of the transforming growth factor-β (TGF-β) superfamily are negatively regulated by inhibitory Smads (I-Smads). Smad7 inhibits signaling by both TGF-β and bone morphogenetic proteins (BMPs), whereas Smad6 inhibits TGF-β signals less effectively. I-Smads have amino-terminal N domains and carboxylterminal Mad homology 2 (MH2) domains. The N domains are essential for specific inhibition of TGF-β signaling by Smad7, whereas the MH2 domains of I-Smads are involved in the inhibition of TGF-β superfamily signals through interaction with type I receptors. Here, we have identified four basic amino acid residues (Lys-312, Lys-316, Lys-401, and Arg-409) in the basic surface of the Smad7 MH2 domain that play important roles in interaction with type I receptors. Mutations of the four basic amino acid residues to acidic residues (K312E, K316E, K401E, and R409E) abolished the interaction of Smad7 with TGF-β type I receptors, inhibition of Smad2 phosphorylation and transcriptional responses induced by TGF-β, and induction of target genes of endogenous activin/Nodal signals in Xenopus early embryos. The K401E and R409E mutants of Smad7 were also unable to interact with BMP type I receptors (BMPR-I), repress the Smad5 phosphorylation and transcription induced by BMP, and effectively inhibit endogenous BMP signals in Xenopus early embryos. However, the K312E and K316E mutants were able to interact with BMPR-I and retained the ability to inhibit BMP signaling. Thus, the MH2 domain of Smad7 plays important roles in specific inhibition of TGF-β superfamily signals through differential interaction with type I receptors. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We aimed to generate equation to predict arterial lactate (a-Lac) using venous lactate (v-Lac) and other lab data. METHODS: A prospective cross-sectional study was conducted on emergency patients in the emergency department for 6 months at a general hospital in Tokyo, Japan. We collected arterial and venous gas analysis data. Patients were eligible for entry into the study if an arterial blood gas analysis was required for appropriate diagnostic care by the treating physician. Univariate linear regression analysis was conducted to generate an equation to calculate a-Lac incorporating only v-Lac. A multivariate forward stepwise logistic regression model (p-value of 0.05 for entry, 0.1 for removal) was used to generate an equation including v-Lac and other potentially relevant variables. Bland-Altman plot was drawn and the two equations were compared for model fitting using R-squares. RESULTS: Seventy-two arterial samples from 72 participants (61% male; mean age, 58.2 years) were included in the study. An initial regression equation was derived from univariate linear regression analysis:'(a-Lac) = -0.259 + (v-Lac) x 0.996'. Subsequent multivariate forward stepwise logistic regression analysis, incorporating v-Lac and Po2, generated the following equation:'(a-Lac) = -0.469+(venous Po2) x 0.005 + (v-Lac) x 0.997'. Calculated R-squares by single and multiple regression were 0.94 and 0.96, respectively. CONCLUSION: v-Lac estimates showed a high correlation with arterial values and our data provide two clinically useful equations to calculate a-Lac from v-Lac data. Considering clinical flexibility, 'Lac = -0.259 + v-Lac x 0.996' might be more useful while avoiding a time-consuming and invasive procedure. [ABSTRACT FROM AUTHOR]

A 74-year-old man was brought to the emergency department (ED) due to a 1-hour course of dyspnea and dysphonia. At arrival in the ED, his airway was managed by bag-valve-mask ventilation. The patient was intubated using a Macintosh laryngoscope with a gum elastic bougie guide. An indirect endoscopic examination revealed prominent epiglottal swelling. Simultaneously, we found a bilateral conjugate deviation to the right and a positive Barré sign for the left arm. Diffusion-weighted magnetic resonance imaging, magnetic resonance angiography, and computed tomography with contrast enhancement revealed a right cerebral hemisphere infarction and dissection of the brachiocephalic artery to the right internal carotid artery. After admission, the patient stated that the movement of his left arm was intact when he became aware of the dyspnea and that he noticed the paralysis of his left arm during transportation to the ED. We believed that these signs resulted from the right hemisphere brain infarction caused by dissection of the brachiocephalic artery to the right internal carotid artery, secondary to the acute epiglottitis. A decrease of intrathoracic pressure due to an upper airway obstruction may cause distention of the intrathoracic arteries and an afterload increase on the left ventricle. The patient was moved to another hospital for rehabilitation on the 20th day after admission. This is the first report of a brain infarction after a dissection of the intrathoracic arteries secondary to acute epiglottitis. Patients with acute epiglottitis should be closely monitored for both airway management and the pathology caused by decreasing intrathoracic pressure. [ABSTRACT FROM AUTHOR]

Summary: Aim: Dexmedetomidine is a highly specific and selective α-2 adrenergic agonist that is now widely used in the intensive care setting. Many intensive care unit (ICU) patients are at risk of respiratory or cardiac arrest. This study was conducted to determine whether dexmedetomidine exhibits a cardioprotective effect on global ischaemia and subsequent myocardial infarction. Methods: Isolated rat hearts were subjected to 30min of global ischaemia followed by 120min reperfusion, with administration of 0, 1 and 10nM dexmedetomidine during the pre-ischaemic period (n =7 each group). Secondly, 1μM yohimbine, an α-2 antagonist, was given during the pre-ischaemic period, alone or in combination with 10nM dexmedetomidine (n =7 each group). Results: Dexmedetomidine administration reduced coronary flow significantly (103.6±4.7%, 77.9±3.7, 63.7±6.1%, of the baseline values for 0, 1 and 10nM dexmedetomidine, respectively), and yohimbine administration reversed this effect (88.0±2.2%). Dexmedetomidine improved the infarct size at each concentration (45.3±3.6, 30.2±3.3, and 21.2±2.3% of the total left ventricular mass for 0, 1, and 10nM dexmedetomidine, respectively), which was also reversed by yohimbine (43.6±1.4%). Conclusion: Dexmedetomidine exhibited a cardioprotective effect on global ischaemia in the isolated rat heart model, which was mediated by α-2 adrenergic stimulation. [Copyright &y& Elsevier]

Aim: This study investigated the value of regional cerebral oxygen saturation (rSO2) monitoring upon arrival at the hospital for predicting post-cardiac arrest intervention outcomes.Methods: We enrolled 1195 patients with out-of-hospital cardiac arrest of presumed cardiac cause from the Japan-Prediction of Neurological Outcomes in Patients Post-cardiac Arrest Registry. The primary endpoint was a good neurologic outcome (cerebral performance categories 1 or 2 [CPC1/2]) 90 days post-event.Results: A total of 68 patients (6%) had good neurologic outcomes. We found a mean rSO2 of 21%±13%. A receiver operating characteristic curve analysis indicated an optimal rSO2 cut-off of ≥40% for good neurologic outcomes (area under the curve 0.92, sensitivity 0.81, specificity 0.96). Good neurologic outcomes were observed in 53% (55/103) and 1% (13/1092) of patients with high (≥40%) and low (<40%) rSO2, respectively. Even without return of spontaneous circulation (ROSC) upon arrival at the hospital, 30% (9/30) of patients with high rSO2 had good neurologic outcomes. Furthermore, 16 patients demonstrating ROSC upon arrival at the hospital and low rSO2 had poor neurologic outcomes. Multivariate analyses indicated that high rSO2 was independently associated with good neurologic outcomes (odds ratio=14.07, P<0.001). Patients with high rSO2 showed favourable neurologic prognoses if they had undergone therapeutic hypothermia or coronary angiography (CPC1/2, 69% [54/78]). However, 24% (25/103) of those with high rSO2 did not undergo these procedures and exhibited unfavourable neurologic prognoses (CPC1/2, 4% [1/25]).Conclusion: rSO2 is a good indicator of 90-day neurologic outcomes for post-cardiac arrest intervention patients. [ABSTRACT FROM AUTHOR]

Abstract: Aim: To investigate the association between regional brain oxygen saturation (rSO2) at hospital arrival and neurological outcomes at 90 days in patients with out-of-hospital cardiac arrest (OHCA). Methods: The Japan-Prediction of neurological Outcomes in patients post cardiac arrest (J-POP) registry is a prospective, multicenter, cohort study to test whether rSO2 predicts neurological outcomes after OHCA. We measured rSO2 in OHCA patients immediately after hospital arrival using a near-infrared spectrometer placed on the forehead with non-blinded fashion. The primary endpoint was “neurological outcomes” at 90 days after OHCA. Results: EMS providers are not permitted to terminate CPR in the field in Japan, and so most patients with OHCA who are treated by EMS personnel are transported to emergency hospitals. Among 1017 OHCA patients, 672 patients including 52 comatose patients with pulses detectable (8%) and 620 cardiac arrest patients (92%) at hospital arrival were enrolled prospectively and consecutively. Twenty-nine patients with good neurological outcome had a significantly higher value of rSO2 at hospital arrival than 643 patients with poor neurological outcome (mean [±SD] 55.6±20.8% vs. 19.7±11.0%, p <0.001). Receiver operating curve analysis indicated an optimal rSO2 cutoff point of >42% for predicting good neurological outcome, with sensitivity 0.79 (95% confidence interval [CI], 0.60–0.92), specificity 0.95 (95% CI, 0.93–0.96), positive predictive value, 0.41 (95% CI, 0.28–0.55), negative predictive value, 0.99 (95% CI, 0.98–1.00), and area under the curve 0.90 (95% CI, 0.88–0.92). Conclusion: The rSO2 at hospital arrival can predict good neurological outcome at 90 days after OHCA. [Copyright &y& Elsevier]

Summary: Intracellular vesicular transport is important for photoreceptor function and maintenance. However, the mechanism underlying photoreceptor degeneration in response to vesicular transport defects is unknown. Here, we report that photoreceptors undergo apoptosis in a zebrafish β-soluble N-ethylmaleimide-sensitive factor attachment protein (β-SNAP) mutant. β-SNAP cooperates with N-ethylmaleimide-sensitive factor to recycle the SNAP receptor (SNARE), a key component of the membrane fusion machinery, by disassembling the cis-SNARE complex generated in the vesicular fusion process. We found that photoreceptor apoptosis in the β-SNAP mutant was dependent on the BH3-only protein BNip1. BNip1 functions as a component of the syntaxin-18 SNARE complex and regulates retrograde transport from the Golgi to the endoplasmic reticulum. Failure to disassemble the syntaxin-18 cis-SNARE complex caused BNip1-dependent apoptosis. These data suggest that the syntaxin-18 cis-SNARE complex functions as an alarm factor that monitors vesicular fusion competence and that BNip1 transforms vesicular fusion defects into photoreceptor apoptosis. [Copyright &y& Elsevier]

Abstract: Aim: To identify patients who can obtain the full benefit from targeted temperature management (TTM) after out-of-hospital cardiac arrest. Methods: We performed a retrospective observational study of comatose patients treated with TTM after an out-of-hospital cardiac arrest from January 2006 to February 2011. Neurological outcome was evaluated with the Glasgow-Pittsburgh Cerebral Performance category (CPC) at discharge and predictors were determined. Results: Of 66 patients studied, 40 (60.6%) survived to neurologically intact discharge (CPC 1 or 2). According to multivariate analysis, predictors of good neurological outcome included arrest-to-first cardiopulmonary resuscitation attempt interval ≤5min, ventricular fibrillation or ventricular tachycardia in the first monitored rhythm, absence of re-arrest before leaving the emergency department, arrest-to-return of spontaneous circulation interval ≤30min and recovery of pupillary light reflex, which were identifiable in the emergency department. Based on this analysis, we developed a seven-point score (5-R score). If the score was ≥5, it predicted good neurological outcome with a sensitivity of 82.5% (95% confidence interval [CI], 67.2–92.7%) and specificity of 92.3% (95% CI, 74.9–99.1%). The negative predictive value of a score ≥4 was 100% (95% CI, 81.5–100%). Our prediction model was validated internally by a bootstrapping technique. Conclusions: The prediction protocol using the 5-R score was associated with good neurological outcome of patients treated with TTM. Therefore, it could be helpful in clinical decision making on whether to initiate cooling. [Copyright &y& Elsevier]