Miracle-dz/UniFAR-FTUs huggingface dataset:
Fontan extracardiac tunnel connection: fenestration or not?

BACKGROUND The fenestration function is by allowing a right-to-left shunt resulting in an increased cardiac index, associated with mild arterial oxygen desaturation. Subsequent transcatheter fenestration closure can be performed after haemodynamic assessment. The purpose of this study was to compare the outcomes of extracardiac connection (EC) with or without fenestration. METHODS Ninety-five consecutive patients diagnosed with univentricular heart disease underwent EC using Gore-Tax conduits at the Department of Children's Heart Center, Justus-Liebig-University Giessen Germany from June 1996 to July 2007. According to EC with or without fenestration, the patients were assigned to two groups (group A with fenestration and group B without fenestration). Mortality, effusions, postoperative mean pulmonary artery pressure, postoperative oxygen saturation, postoperative thrombosis, postoperative neurological problems, and the postoperative loss of sinus rhythm were compared. In group A, 23 patients had fenestration closed interventionally after a mean time of 20-22 months. RESULTS Mortality and postoperative mean pulmonary artery pressure in group B (3 and (15.1 +/- 3.4) mmHg, respectively) were significantly higher than group A (0 and (13.2 +/- 2.8) mmHg, respectively). Postoperative oxygen saturation, postoperative thrombosis, postoperative neurological problems, and the postoperative loss of sinus rhythm did not differ between cohorts. CONCLUSIONS Fenestrating an extracardiac tunnel seems to improve acute postoperative mortality by rising cardiac output. The induced right-to-left shunt shows no morbidity postoperatively. If a stabilized chronic hemodynamic situation is achieved, an interventional closure of the fenestration can be performed to advance the arterial saturation and improve the exercise tolerance of the patients.
Central Angiotensin-II Increases Blood Pressure and Sympathetic Outflow via Rho Kinase Activation in Conscious Rabbits

Elevated sympathetic tone and activation of the renin–angiotensin system are pathophysiologic hallmarks of hypertension, and the interactions between these systems are particularly deleterious. The importance of Rho kinase as a mediator of the effects of angiotensin-II (AngII) in the periphery is clear, but the role of Rho kinase in sympathoexcitation caused by central AngII is not well established. We hypothesized that AngII mediates its effects in the brain by the activation of the RhoA/Rho kinase pathway. Chronically instrumented, conscious rabbits received the following intracerebroventricular infusion treatments for 2 weeks via osmotic minipump: AngII, Rho kinase inhibitor Fasudil, AngII plus Fasudil, or a vehicle control. AngII increased mean arterial pressure over the course of the infusion, and this effect was prevented by the coadministration of Fasudil. AngII increased cardiac and vascular sympathetic outflow as quantified by the heart rate response to metoprolol and the depressor effect of hexamethonium; coadministration of Fasudil abolished both of these effects. AngII increased baseline renal sympathetic nerve activity in conscious animals and impaired baroreflex control of sympathetic nerve activity; again Fasudil coinfusion prevented these effects. Each of these end points showed a statistically significant interaction between AngII and Fasudil. Quantitative immunofluorescence of brain slices confirmed that Rho kinase activity was increased by AngII and decreased by Fasudil. Taken together, these data indicate that hypertension, elevated sympathetic outflow, and baroreflex dysfunction caused by central AngII are mediated by Rho kinase activation and suggest that Rho kinase inhibition may be an important therapeutic target in sympathoexcitatory cardiovascular diseases.
Complete mitochondrial genome of Cygnus cygnus (Aves, Anseriformes, Anatidae)

Abstract In this study, the complete mitochondrial genome of Cygnus cygnus (Aves, Anseriformes, Anatidae) was sequenced. The genome, consisting of 16 724 base pairs (bp), encoded 13 protein coding genes (PCGs), two ribosomal RNAs (rRNAs), 22 transfer RNAs (tRNAs), and a control region (CR). Two rRNA genes for 12S rRNA (991 bases) and 16S rRNA (1608 bases) are located between tRNA-Phe and tRNA-Leu (UUR) and divided by the tRNA-Val. The CR, of 1156 bp in length, is located between tRNA-Glu and tRNA-Phe. The overall base composition of C. cygnus is G + C: 47.2%, A + T: 52.8%, apparently with a slight AT bias. Phylogenetic analysis showed that the C. cygnus was closed to Cygnus columbianus.
Ultrasound non-invasive measurement of intracranial pressure in neurointensive care: A prospective observational study

Background The invasive nature of the current methods for monitoring of intracranial pressure (ICP) has prevented their use in many clinical situations. Several attempts have been made to develop methods to monitor ICP non-invasively. The aim of this study is to assess the relationship between ultrasound-based non-invasive ICP (nICP) and invasive ICP measurement in neurocritical care patients. Methods and findings This was a prospective, single-cohort observational study of patients admitted to a tertiary neurocritical care unit. Patients with brain injury requiring invasive ICP monitoring were considered for inclusion. nICP was assessed using optic nerve sheath diameter (ONSD), venous transcranial Doppler (vTCD) of straight sinus systolic flow velocity (FVsv), and methods derived from arterial transcranial Doppler (aTCD) on the middle cerebral artery (MCA): MCA pulsatility index (PIa) and an estimator based on diastolic flow velocity (FVd). A total of 445 ultrasound examinations from 64 patients performed from 1 January to 1 November 2016 were included. The median age of the patients was 53 years (range 37–64). Median Glasgow Coma Scale at admission was 7 (range 3–14), and median Glasgow Outcome Scale was 3 (range 1–5). The mortality rate was 20%. ONSD and FVsv demonstrated the strongest correlation with ICP (R = 0.76 for ONSD versus ICP; R = 0.72 for FVsv versus ICP), whereas PIa and the estimator based on FVd did not correlate with ICP significantly. Combining the 2 strongest nICP predictors (ONSD and FVsv) resulted in an even stronger correlation with ICP (R = 0.80). The ability to detect intracranial hypertension (ICP ≥ 20 mm Hg) was highest for ONSD (area under the curve [AUC] 0.91, 95% CI 0.88–0.95). The combination of ONSD and FVsv methods showed a statistically significant improvement of AUC values compared with the ONSD method alone (0.93, 95% CI 0.90–0.97, p = 0.01). Major limitations are the heterogeneity and small number of patients included in this study, the need for specialised training to perform and interpret the ultrasound tests, and the variability in performance among different ultrasound operators. Conclusions Of the studied ultrasound nICP methods, ONSD is the best estimator of ICP. The novel combination of ONSD ultrasonography and vTCD of the straight sinus is a promising and easily available technique for identifying critically ill patients with intracranial hypertension.
Electrical Degradation of InAlN/GaN HEMTs Operating Under ON Conditions

The degradation of InAlN/GaN high-electron-mobility transistors (HEMTs) for millimeter-wave applications has been examined under on conditions. Two dominant permanent degradation mechanisms have been identified as well as two trapping mechanisms which affect the device characteristics in different ways. Under high-voltage, low-current stress conditions, we have observed permanent enhancement in the maximum drain current IDmax that arises from a negative shift in threshold voltage VT. We attribute this mechanism to depassivation of hydrogenated defects. Under the same stress conditions, there is prominent and reversible hot-electron trapping on the drain side of the device that brings IDmax down and increases the drain resistance. Under low-voltage high-current stress conditions, there is a visible permanent reduction in IDmax and a positive shift in VT. This is also the signature of-high temperature stress under unbiased conditions and is attributed to gate sinking.
Additionality, Transactional Barriers and the Political Economy of Climate Change

Stabilization of greenhouse gases at sustainable levels is the objective of the FCCC. Strategies to achieve this aim have been the object of intense debate. This paper focuses on one emissions trading system under scrutiny, Joint Implementation (JI). The basic premise of JI is that one nation party can satisfy its obligations to control emissions by financing emission mitigation in another nation party. Such an approach can optimize access to least cost mitigation options, and predicts collective participation even in the absence of centralized determination of universal quotas. A key issue for JI is the concept of additionality. "Business as usual" trajectories provide a baseline against which additionality is measured. Accurate estimation of baselines needs to take into proper account institutional and organizational transaction costs. Hence, the implementation of a climate change system incorporating JI as a core element requires a greater understanding of the incentives and barriers that underlie the patterns of infrastructure development in rapidly growing economies. Readers should note that all of this paper's analyses and conclusions related to JI apply equally to the new clean development mechanism established by article 12 of the Kyoto protocol.
Potentiation of kappa-opioid receptor agonist-induced analgesia and hypothermia by fluoxetine.

The effect of fluoxetine, a selective 5-HT reuptake inhibitor on the analgesic and hypothermic response of trans-(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]-benzeneacetamide methane sulphonate (U-50,488H) and (+/-)-trans-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl] benzo[b] thiophene-4-acetamide (PD 117302), kappa-opioid receptor agonists, was determined in female Sprague-Dawley rats using the tail-flick method and telethermometer, respectively. Intraperitoneal injections of U-50,488H (U50) and PD 117302 (PD117) produced a dose-dependent analgesic and hypothermic response. Fluoxetine (10 mg/kg, i.p.) by itself did not produce an analgesic response. The analgesic response to U50 (10, 20, and 40 mg/kg, i.p.) and PD117 (7.5, 15, and 22.5 mg/kg, i.p.) was potentiated by fluoxetine injected intraperitoneally 60 min prior to the injection of kappa-opioid agonists. Similarly, the hypothermic response of U50 (20 and 40 mg/kg, i.p.) and PD117 (7.5, 15, and 22.5 mg/kg, i.p.) was potentiated by fluoxetine. The results indicate that selective kappa-opioid receptor agonists-induced analgesia and hypothermia is potentiated by fluoxetine, suggesting the role of extracellular 5-HT in the kappa-opioid receptor-mediated analgesia and hypothermia.
Non-Technological and Non-Economic Innovations. Contributions to a Theory of Robust Innovation, 2nd Edition

Although the label innovation is applied to almost everything, with even the diffusion of innovations to society being called innovation, innovation research remains focused on bringing technology to the economic market. This dissonance provoked the central questions discussed at the 2nd International Conference on Indicators and Concepts of Innovation (ICICI). What are non-technological and non-economic innovations? What impact do these innovations have on the economy? Are there actually purely technological or economic innovations? Consisting of selected answers to these questions, this volume presents international approaches beyond the technology to market mainstream of innovation research as well as analyses of socially robust innovations that succeed in both economic and non-economic markets and are hence more sustainable and more profitable. The 2nd ICICI has been supported by the SCOPES program of the Swiss National Science Foundation.
Risk‐adjusted surgical audit with the POSSUM scoring system in a developing country

The Physiological and Operative Severity Score for the enUmeration of Mortality and morbidity (POSSUM) is an objective and appropriate scoring system for risk‐adjusted comparative general surgical audit. This score was devised in the UK and has been used widely, but application of POSSUM to centres outside the UK has been limited, especially in developing countries. This prospective study validated its application in a surgical practice with a different population and level of resources.
Changing Rates of Morbidity and Mortality in Obstructive Sleep Apnea Surgery

Objective Whereas uvulopalatopharyngoplasty (UPPP) was the standard surgical procedure for obstructive sleep apnea prior to 2007, multilevel surgery has become the standard since that time. This study compares morbidity and mortality rates of the stand-alone UPPP with those of multilevel sleep surgery that includes UPPP. Methods Patients undergoing UPPP between 2007 and 2014 were identified in the American College of Surgeons National Surgical Quality Improvement Program database. UPPP was defined by Current Procedural Terminology codes 42145 and 42950. Primary outcomes were incidence of morbidity and mortality. Rates were compared between a control group with UPPP only and a group with multilevel surgery. Results A total of 2674 cases were analyzed. The incidence of complications in the UPPP-only group was 1.6% (0.09% fatal); in the multilevel surgery group, 4.63% (0.19% fatal). The difference in overall and nonfatal complications is statistically significant (P < .01); however, values for fatal complications are too low for comparison. There is a statistically significant (P < .01) positive correlation (R2 = 0.92) between year of operation and rate of complications, with increased incidence of complications in more recent years. Discussion Complication rates for multilevel sleep surgery are higher than those of stand-alone UPPP, and overall complication rates have been increasing in recent years. As UPPP supplemented with multilevel surgery is now the standard surgical treatment for most cases of obstructive sleep apnea-hypopnea syndrome, historical complication rates based predominantly on patients undergoing UPPP only underestimate complication rates of modern sleep surgery. Implications for Practice It is reasonable to inform patients that multilevel procedures bring an increased risk of complications, and patient selection should be guided accordingly.
The microbial metabolism of condensed (+)-catechins by rat-caecal microflora.

The metabolism of 2,3-trans-3,4-trans-3,5,7,3',4'-pentahydroxy-4-(2,4,6-trihydrox yphenyl)-flavan and 2,3-trans-3,4-trans-3,5,7,3',4',-pentahydroxy-4-(2,3-trans-3,5,7,3 ', 4'-pentahydroxyflavanyl-[8])-flavan in vitro by rat-caecal microflora was investigated. Metabolites were extracted and enriched by column chromatography and preparative h.p.l.c. , while structural determination was carried out using comparative g.l.c. -mass spectrometry and p.m. r. spectrometry. The metabolites identified were derivatives of benzoic acid, phenylacetic acid, phenylpropionic acid and phenyllactic acid in addition to phloroglucinol, delta-(3-hydroxyphenyl)-gamma-valerolactone and 1-(3-hydroxyphenyl)-3-(2,4,6-trihydroxyphenyl)-propan-2-ol. An additional metabolic route, which differs from the expected severance of the (+)-catechin-phloroglucinol bond and well-documented total heterocyclic ring degradation of flavanoids, is proposed.
Acute generalized exanthematous pustulosis associated with Helicobacter pylori eradication therapy with elevated serum procalcitonin

259 mediates cutaneous healing by regulatory T cells supports this idea [7, 8]. Reports on EPDS-like eruptions under treatment with EGFR-I (such as gefitinib or cetuximab) further corroborate the role of EGFR in the onset of EPDS [9, 10]. Two types of eruptions associated with EGFR-I exist; acneiform eruptions (or erythematous papulopustular eruptions) and scarring folliculitis [2-4]. In our patient, we found scarring folliculitis but no comedo formation in the affected area. However, the distinction between EPDS and EGFRI-associated eruptions remains subtle. In summary, we describe a patient with EPDS succeeding herpes zoster infection, which was improved by the discontinuation of concurrent afatinib. Our observation suggests an involvement of the EGFR pathway in the onset and development of EPDS. However, the improvement of the eruption after discontinuation of EGFR-I afatinib and the histopathological similarity between EPDS and EGFRI-associated eruption argue in favour of the diagnosis of EPDS in our case. Observation of additional cases and histological studies will help to better distinguish EPDS from acneiform eruptions due to EGFR-I.
Factors Influencing Allopurinol Initiation in Primary Care

Despite guidance on appropriate initiation, urate-lowering therapy is prescribed for only a minority of patients with gout. Electronic health records for 8,142 patients with gout were used to investigate the effect of age, sex, comorbidities, number of consultations, and meeting internationally agreed eligibility criteria on time to allopurinol initiation. Time to first prescription was modeled using multilevel Cox proportional hazards regression. Allopurinol initiation was positively associated with meeting eligibility criteria at diagnosis of gout, but negatively associated with becoming eligible after diagnosis. Managing gout as a chronic disease, with regular reviews to discuss allopurinol treatment, may reduce barriers to treatment.
Vascular smooth muscle cells efficiently activate a new proteinase cascade involving plasminogen and fibronectin

The plasminogen/plasmin system is involved in vascular wall remodeling after injury, through extracellular matrix (ECM) degradation and proteinase activation. Vascular smooth muscle cells (VSMCs) synthesize various components of the plasminogen/plasmin system. We investigated the conversion of plasminogen into plasmin in primary cultured rat VSMCs. VSMCs efficiently converted exogenous plasminogen into plasmin in a time‐ and dose‐dependent manner. We measured plasmin activity by monitoring the hydrolysis of Tosyl‐G‐P‐R‐Mca, a fluorogenic substrate of plasmin. Cell‐mediated plasmin activation was associated with the degradation of ECM, as revealed by fibronectin proteolysis. Plasmin also activated a proteinase able to hydrolyze Mca‐P‐L‐G‐L‐Dpa‐A‐R‐NH2, a fluorogenic substrate of matrix metalloproteinases (MMPs). However, this proteinase was not inhibited by an MMP inhibitor. Furthermore, this proteinase displayed similar biochemical and pharmacological properties to fibronectin‐proteinase, a recently identified zinc‐dependent metalloproteinase located in the gelatin‐binding domain of fibronectin. These results show that VSMCs convert exogenous plasminogen into plasmin in their pericellular environment. By hydrolyzing matrix protein plasmin activates a latent metalloproteinase that differs from MMP, fibronectin‐proteinase. This metalloproteinase may participate to vascular wall remodeling, in concert with other proteinases. J. Cell. Biochem. 88: 1188–1201, 2003. © 2003 Wiley‐Liss, Inc.
Associations of Insulin and IGFBP-3 with Lung Cancer Susceptibility in Current Smokers.

BACKGROUND The epidermal growth factor receptor (EGFR) signaling network is involved in lung carcinogenesis. This study examined whether ligands that activate or suppress the EGFR signaling network were associated with lung cancer risk in ever smokers. METHODS A nested case-control study within the Women's Health Initiative assessed baseline plasma levels of insulin, insulin-like growth factor (IGF)-1, insulin-like growth factor binding protein (IGFBP)-3, interleukin (IL)-6, hepatocyte growth factor (HGF), and nerve growth factor (NGF) in 1143 ever-smoking lung cancer cases and 1143 controls. Leptin was measured as an adiposity biomarker. Conditional logistic regression was used in data analyses. RESULTS Leptin was inversely associated with lung cancer risk (odds ratio [ORcontinuous] per Ln [pg/mL] = 0.85, 95% confidence interval [CI] = 0.74 to 0.98). After adjusting for adiposity and other risk factors, null associations were found for IL-6, HGF, and NGF. In current smokers, but not former smokers, high insulin levels were associated with increased lung cancer risk (OR for 4th quartile vs others [ORq4] = 2.06, 95% CI = 1.30 to 3.26) whereas IGFBP-3 had a linear inverse association (ORcontinuous per μg/mL = 0.64, 95% CI = 0.41 to 0.98). The insulin association was consistent across subgroups defined by body mass index and histological type, but the IGFBP-3 association was specific to small cell lung cancer. There was a modest positive association between IGF-1 and lung cancer risk in current smokers (ORq4 = 1.44, 95% CI = 0.90 to 2.29). CONCLUSIONS Independent of obesity, high insulin levels but reduced levels of IGFBP-3 were associated with increased lung cancer risk in current smokers.
Optimal Inflation Targets, 'Conservative' Central Banks, and Linear Inflation Contracts

Inflation target regimes (like those of New Zealand, Canada, U.K., Sweden and Finland) are interpreted as having explicit inflation targets and implicit output/unemployment targets. Without output-unemployment persistence delegation of monetary policy to a discretionary instrument-independent central bank with an optimal inflation target can eliminate the discretionary inflation bias, mimic the optimal linear inflation contract suggested by Walsh and extended by Persson and Tabellini, and achieve the equilibrium corresponding to an optimal rule with commitment. Thus an `inflation target- conservative' central bank with an inflation target equal to the socially best inflation rate less any inflation bias dominates a Rogoff weight-conservative central bank with increased weight on inflation stabilizatiojn, which suboptimally increases output/unemployment variability. With output/ unemployment persistence, a constant inflation target is equivalent to a constant linear inflation contract. They can both eliminate the average inflation bias but not the state-contingent part of the inflation bias. Inflation variability is too high, and output variability too low, compared to the equilibrium corresponding to an optimal rule. An optimal state- contingent inflation target can remove all inflation bias, but in contrast to an optimal state-contingent linear inflation contract it still leaves inflation variability too high. Delegation with an optimal state-contingent inflation target to a Rogoff `weight-conservative' central bank can then achieve the equilibrium corresponding to an optimal rule. Inflation targets may on average be exceeded, and they may have imperfect credibility, but they may usefully reduce inflation, and they appear much easier to implement.