Miracle-dz/UniFAR-FTUs huggingface dataset:
Intraoperative minimal acute normovolemic hemodilution in patients undergoing coronary artery bypass surgery.

BACKGROUND & OBJECTIVE Efficacy of minimal acute normovolemic hemodilution (ANH) in avoiding homologous blood transfusion during cardiovascular surgery remains controversial. Postoperative bleeding and transfusion remain a source of morbidity and cost after open heart operations. Our objective was to evaluate the impact of minimal ANH on blood transfusion requirements during open cardiovascular surgery using cardiopulmonary bypass (CPB). METHODS This study was a randomized controlled trial. One hundred one patients scheduled for elective coronary artery bypass graft (CABG) under cardiopulmonary bypass in October 2007 through March 2008 in Imam Khomeini hospital were randomly assigned to a control group (standard care, no = 47) or an ANH or study group (no = 54). We used minimal ANH (representing 10% of patients' blood volume). Mean 490 +/- 50 mL of fresh autologous blood was removed after induction of anesthesia and reinfused at the end of CPB. The blood transfusion guidelines were uniformly applied to all patients. RESULTS Significant decrease in the number of red blood cell units transfused per patient per group (1.39 +/- 1.0 and 2.551.9 +/- units; p < 0.0001) in the ANH group versus the control group was observed. Conversely, chest tube output, postoperative hematocrits, and platelet count did not differ between two groups. Percentage of patients in whom allogeneic red blood cells were transfused was 44% in study group versus 76% in control group; (p < 0.01). No patient was transfused with platelet concentrates or fresh frozen plasma. CONCLUSIONS Minimal ANH is safe and cost effective and its routine use in eligible patients is therefore justified. Intraoperative autologous blood donation in CABG surgery decreased perioperative allogeneic blood requirement. However, the removal and reinfusion of about one unit autologous blood had no effect on postoperative bleeding or platelet count.
Broadband Doherty Power Amplifier via Real Frequency Technique

A comprehensive method of designing a broadband Doherty power amplifier is presented in this paper. The essential limitations of bandwidth extension of a Doherty power amplifier are discussed based on the proposed structure of the Doherty power amplifier, which also takes the output matching networks of both sub-amplifiers into account. The broadband matching is realized by applying the simplified real frequency technique with the desired frequency-dependent optimum impedances. GaN transistors were selected to implement the circuit structure.
Authentication and Key Establishment in Dynamic Wireless Sensor Networks

When a sensor node roams within a very large and distributed wireless sensor network, which consists of numerous sensor nodes, its routing path and neighborhood keep changing. In order to provide a high level of security in this environment, the moving sensor node needs to be authenticated to new neighboring nodes and a key established for secure communication. The paper proposes an efficient and scalable protocol to establish and update the authentication key in a dynamic wireless sensor network environment. The protocol guarantees that two sensor nodes share at least one key with probability 1 (100%) with less memory and energy cost, while not causing considerable communication overhead.
Trapping a Knot into Tight Conformations by Intra-Chain Repulsions

Knots can occur in biopolymers such as DNA and peptides. In our previous study, we systematically investigated the effects of intra-chain interactions on knots and found that long-range repulsions can surprisingly tighten knots. Here, we use this knowledge to trap a knot into tight conformations in Langevin dynamics simulations. By trapping, we mean that the free energy landscape with respect to the knot size exhibits a potential well around a small knot size in the presence of long-range repulsions, and this potential can well lead to long-lived tight knots when its depth is comparable to or larger than thermal energy. We tune the strength of intra-chain repulsion such that a knot is weakly trapped. Driven by thermal fluctuations, the knot can escape from the trap and is then re-trapped. We find that the knot switches between tight and loose conformations—referred to as “knot breathing”. We use a Yukawa potential to model screened electrostatic interactions to explore the relevance of knot trapping and breathing in charged biopolymers. We determine the minimal screened length and the minimal strength of repulsion for knot trapping. We find that Coulomb-induced knot trapping is possible to occur in single-stranded DNA and peptides for normal ionic strengths.
New monoclonal antibody (4E9R) identifies mouse neural crest cells

In order to analyze migration patterns of mouse neural crest cells, we produced a rat anti‐mouse monoclonal antibody (4E9R) which identifies these cells. The distribution of 4E9R‐immunoreactive cells was examined in migratory stages of mouse neural crest cells, ranging from embryonic day (Ed) 8.5 to 10.5. In the cephalic region of Ed 8.5 embryos, some mesencephalic mesenchymal cells close to neural folds were 4E9R‐positive. In Ed 9.0–9.5 embryos, streams of 4E9R‐immunoreactive cells extending from cranial neural tubes to maxillary processes and to first visceral arches were found in the lateral region and some of these cells were localized in presumptive trigeminal ganglia. In the same embryonic stages, 4E9R‐positive cells were present in mesenchymal cells around the optic and otic vesicles. In the trunk region of Ed 9.5–10.5 embryos, 4E9R‐positive cell masses were observed in dorsolateral spaces adjacent to neural tubes. The presence of 4E9R‐immunoreactive cells in somitic segments was restricted within the anterior halves and these cells were seen under the dermomyotome and/or in the medial portion of the sclerotome. These cells colonized in presumptive dorsal root ganglia and in the surroundings of the dorsal aorta, the embryonic area in which sympathetic ganglia are formed. 4E9R‐positive cells were also found just under the epidermis. These observations indicate that the distribution of 4E9R‐positive cells is similar to that of amniote neural crest cells reported previously. Furthermore, the data suggest that the migratory behavior of mouse neural crest cells at trunk levels may be different between rostral and caudal levels within an anterior half of the sclerotome, and that sympathetic ganglia may be formed by neural crest cells migrating along “ventromedial pathways” as well as “ventrolateral pathways” at hindlimb‐bud levels of mouse embryos. In primary cultures of mouse neural crest cells, approximately 80% of the cells were 4E9R‐positive on culture day 2. Further, we have shown in cultures treated with colchicine or cytochalasin B that 4E9R antigens are present in intermediate filaments. When image analysis with a confocal laser scanning microscope was performed on primary cultures of mouse neural crest cells, the intracellular localization of 4E9R antigens in these cells was comparable to that of vimentin, which is a typical intermediate filament in most mesenchymal cells in embryonic stages examined. Since the distribution of 4E9R‐positive cells and anti‐vimentin‐immunoreactive cells was different in mouse embryos, it is suggested that 4E9R antigens are vimentin‐related and specifically expressed in a few cell types including mouse neural crest cells. These results indicate that a rat anti‐mouse monoclonal antibody 4E9R is useful for the identification of mouse neural crest cells during the migratory stages. © 1996 Wiley‐Liss, Inc.
Influence of a Subanesthetic Concentration of Halothane on the Ventilatory Response to Step Changes into and out of Sustained Isocapnic Hypoxia in Healthy Volunteers

Backgroundin humans the ventilatory response to isocapnic hypoxia is biphasic: an initial increase in minute ventilation (&OV0312;E) from baseline, the acute hypoxic response, is followed after 3–5 min by a slow ventilatory decay, the hypoxic ventilatory decline, and a new steady state, 25–40% greater than baseline &OV0312;E, is reached in about 15–20 min. The transition from 20 min of isocapnic hypoxia into normoxia results in a rapid decrease in &OV0312;E, the off-response. in humans, halothane, at subanesthetic concentrations, is known to decrease the acute hypoxic response. in order to investigate the effects of halothane on sustained hypoxia we quantified the effects of 0.15 minimum alveolar concentration halothane on the ventilatory response at the onset of 20 min of hypoxia and at the termination of 20 min of hypoxia by normoxia in healthy volunteers. MethodsStep changes in end-tidal oxygen tension were performed against a background of constant mild hypercapnia (end-tidal carbon dioxide tension about 1 mmHg above individual resting values) in fourteen male subjects. The end-tidal oxygen tension was forced as follows: 5–10 min at 110 mmHg, 20 min at 44 mmHg, and 10 min at 110 mmHg. in each subject we performed one trial before and one during 0.15 minimum alveolar concentration halothane administration. ResultsTen responses into hypoxia and nine out of hypoxia were considered for analysis. All control trials were performed during wakefulness. Using behavioral characteristics, the central nervous system arousal state of the subjects during halothane inhalation was defined as “anesthsia-induced hypnosis. ” The acute hypoxic response averaged 10.4 ± 4.71/min for control versus 3.7 ± 2.4 1/min for halothane trials (P < 0.01). The hypoxic ventilatory decline was 4.8 ± 2.5 1/min versus 3.9 ± 2.9 1/min (NS), the off-response was 6.7 ± 3.2 1/ min versus 3.7 ± 3.0 1/min (P < 0.05) for control versus halothane, respectively. All values are mean ± SD. ConclusionsOur results indicate that halothane caused &OV0312;E to be less than control levels during acute and sustained hypoxia as well as when sustained hypoxia is replaced by normoxia. it is argued that the depression of &OV0312;E during acute hypoxia is attributed to an effect of halothane on the peripheral chemoreceptors. During sustained hypoxia halothane had no effect on the magnitude of the hypoxic ventilatory decrease, which is probably related to an increase by halothane of inhibitory neuromodulators within the central nervous system. With halothane, the ventilatory decrease when sustained hypoxia is replaced by normoxia is related to the removal of the hypoxic drive at the site of the peripheral chemoreceptors.
Online Condition Monitoring of Onboard Traction Transformer Core Based on Core-Loss Calculation Model

According to the special working condition in the commutation region of the traction grid, a novel technique of online core-loss measurement for the electric locomotive onboard traction transformer is proposed to noninvasively monitor the status of the magnetic core in real time. Meanwhile, a new modeling approach is also put forward for the equivalent nonlinear magnetizing inductance <inline-formula><tex-math notation="LaTeX">$L_{M}$</tex-math> </inline-formula> of the magnetic core. First, a no-load test under 31 kV is implemented on a healthy traction transformer, and the measured transient terminal voltages and currents are then filtered and downsampled by the comprehensive test and fault diagnosis system of electric locomotive traction transformer. Next, the magnetizing inductance <inline-formula><tex-math notation="LaTeX">$L_{M}$</tex-math></inline-formula> is modeled as the ratio of “the derivative of main flux linkage <italic>λ<sub>p</sub></italic> with respect to time” over “the derivative of magnetizing current <inline-formula><tex-math notation="LaTeX">$i_{m}$</tex-math> </inline-formula> with respect to time. ” After that the proposed <inline-formula><tex-math notation="LaTeX"> $L_{M}$</tex-math></inline-formula> model is verified by comparing with the experimental results and two other models. Finally, the proposed technique for online estimation of core loss is applied on a normal onboard traction transformer and a downscaled testing transformer with different severity of interlaminar fault. The experimental results approximately match the theoretical calculation, and the online estimated values of core loss show sharply rising trend under incipient fault.
Increased morbidity from nasopharyngeal carcinoma and chronic pharyngitis or sinusitis among workers at a newspaper printing company

Objectives: To determine the association between printing works and nasopharygeal carcinoma as well as other diseases. Methods: Demographic data were obtained for those who had worked in a particular newspaper company since its establishment in 1950. Through access to the data bank of the hospital records of the Labor Insurance Bureau for 1985–94, all workers were identified who had been admitted to hospital during their employment in the newspaper company. Multiple logistic regressions were performed to estimate the adjusted morbidity odds ratio (OR) for various diseases among the printing workers with cardiovascular diseases as the reference diseases. Biopsy specimens from patients with nasopharyngeal carcinoma were all subjected to in situ hybridisation of Epstein-Barr virus (EBV), and colocalisation of EBV and secretor component protein. Results: Of the 1564 people who had worked in this company, 579 of them were admitted to hospital at least once. Five out of 144 printing workers admitted to hospital were diagnosed with nasopharyngeal carcinoma compared with none of the other 435 non-printing workers admitted to hospital. The morbidity OR for nasopharyngeal carcinoma in printing workers was 57.0 (95% confidence interval (95% CI) 2.8 to 1155.3). The morbidity OR for benign skin tumours was 28.0 (95% CI 2.7 to 293.1). Chronic pharyngitis or sinusitis also showed significant relations with printing works with a morbidity OR 29.4 (95% CI 1.7 to 514.7). Using all other diseases as the reference diseases for calculation of morbidity ORs still showed a similar trend. In situ hybridisation of EBV encoded small nuclear RNA-1 (EBER-1) showed tumour cells free of the EBV in each biopsy specimen. Colocalisation of EBER-1 and secretor component showed that some tumour cells contained both secretor component and EBV signal in each case. Conclusion: Printing works are associated with an increased risk of nasopharyngeal carcinoma, benign skin tumours, chronic pharyngitis or sinusitis, chronic liver diseases, and mechanical injuries. Induction of the development of nasopharyngeal carcinoma is probably not related to EBV infection in these patients.
Trust in new decision aid systems

One of the main challenges to face concerning the safe utilization of new technologies in complex systems concerns the level of trust the operators have in the system. Danger exists when the operators have a low level of trust in it, as well as it also exists when they overtrust the system. This paper presents an extensive review of theoretical, empirical, and experimental studies on trust in systems. Its goal is to help system designers by proposing a set of design rules and guidelines on how to support appropriate trust tuning in new decision aid systems.
The Role of Autonomic Factors in Sudden Unexpected Death in

Sudden unexpected death in epilepsy (SUDEP) is the most important direct epilepsy-related cause of death. Despite its growing recognition amongst clinicians caring for patients with epilepsy, the exact pathophysiologic mechanisms behind SUDEP have not yet been fully elucidated. However, autonomic effects of seizures are thought to most likely to contribute to sudden unexpected death. Such autonomic effects may affect the heart. These include peri-ictal tachycardia, bradycardia, asystole, repolarization abnormalities, and/or reduced heart rate variability. Respiration may also be affected by seizures, with resulting hypoventilation, apnea, and hypoxemia. More recently, postictal generalized EEG suppression (PGES) has been hypothesized to be an electrophysiologic marker of increased SUDEP risk. If the cortical neuronal inhibition suggested by PGES affects deeper subcortical and brainstem structures, it may interfere with respiratory drive and result in apnea, putting patients at risk for sudden death. Given that SUDEP occurs less frequently than any peri-ictal autonomic disturbance in isolation, it is possible that death only occurs when several precipitating factors come together in a “perfect storm. ” Increasing our understanding of SUDEP will require further exploration of ictal and interictal autonomic dysfunction in patients with seizures. It is only through such research that we may one day understand SUDEP enough to fully prevent it.
Trichostatin A Rescues the Disrupted Imprinting Induced by Somatic Cell Nuclear Transfer in Pigs

Imprinting disorders induced by somatic cell nuclear transfer (SCNT) usually lead to the abnormalities of cloned animals and low cloning efficiency. Histone deacetylase inhibitors have been shown to improve gene expression, genomic methylation reprogramming and the development of cloned embryos, however, the imprinting statuses in these treated embryos and during their subsequent development remain poorly studied. In this study, we investigated the dynamics of H19/Igf2 methylation and transcription in porcine cloned embryos treated with trichostatin A (TSA), and examined H19/Igf2 imprinting patterns in cloned fetuses and piglets. Our results showed that compared with the maintenance of H19/Igf2 methylation in fertilized embryos, cloned embryos displayed aberrant H19/Igf2 methylation and lower H19/Igf2 transcripts. When TSA enhanced the development of cloned embryos, the disrupted H19/Igf2 imprinting was largely rescued in these treated embryos, more similar to those detected in fertilized counterparts. Further studies displayed that TSA effectively rescued the disrupted imprinting of H19/Igf2 in cloned fetuses and piglets, prevented the occurrence of cloned fetus and piglet abnormalities, and enhanced the full-term development of cloned embryos. In conclusion, our results demonstrated that aberrant imprinting induced by SCNT led to the abnormalities of cloned fetuses and piglets and low cloning efficiency, and TSA rescued the disrupted imprinting in cloned embryos, fetuses and piglets, and prevented the occurrence of cloned fetus and piglet abnormalities, thereby improving the development of cloned embryos. This study would have important implications in improving cloning efficiency and the health of cloned animals.
An Intestinal Epithelium-Specific Cytochrome P450 (P450) Reductase-Knockout Mouse Model: Direct Evidence for a Role of Intestinal P450s in First-Pass Clearance of Oral Nifedipine

To determine the in vivo function of intestinal cytochrome P450 (P450) enzymes, we have generated an intestinal epithelium (IE)-specific P450 reductase gene (Cpr) knockout mouse model (designated IE-Cpr-null). In the IE-Cpr-null mouse, CPR expression was abolished in IE cells; however, CPR expression was not altered in other tissues examined. The loss of CPR expression in the small intestine (SI) led to increased expression of several P450 proteins examined, including CYP1A1, CYP2B, CYP2C, and CYP3A. It is interesting to note that the expression of CYP1A1 was also increased in the liver, kidney, and lung of the IE-Cpr-null mice compared with wild-type (WT) littermates, a result strongly supporting the notion that SI metabolism of putative dietary CYP1A1 inducers can influence the systemic bioavailability of these inducers. The rates of SI microsomal metabolism of nifedipine (NFP) in the IE-Cpr-null mice were ∼10% of the rates in WT littermates, despite the compensatory expression of multiple P450 enzymes in the SI. Furthermore, the area under the concentration-time curve (AUC) values for blood NFP (dosed at 10 mg/kg) levels were 1.6-fold higher in IE-Cpr-null mice than in WT littermates when NFP was given orally; in contrast, the AUC values were comparable for the two strains when NFP was given intravenously. This result directly showed that P450-catalyzed NFP metabolism in the SI plays an important role in the first-pass clearance of oral NFP. Our findings indicate that the IE-Cpr-null mouse model can be used to study the in vivo function of intestinal P450 enzymes in the clearance of oral drugs and other xenobiotics.
NKG 2 D-dependent Natural Killer Cell Cytotoxicity Different Histotypes : Analysis of Tumor Susceptibility to UL 16-Binding Protein Expression on Tumor Cell Lines of Major Histocompatibility Complex Class I-related Chain A and Updated

NKG2D, together with NKp46 and NKp30, represents a major triggering receptor involved in the induction of cytotoxicity by both resting and activated human natural killer cells. In this study, we analyzed the expression and the functional relevance of MHC class I-related chain A (MICA) and UL16 binding protein (ULBP), the major cellular ligands for human NKG2D, in human tumor cell lines of different histological origin. We show that MICA and ULBP are frequently coexpressed by carcinoma cell lines, whereas MICA is expressed more frequently than ULBP by melanoma cell lines. Interestingly, the MICA ULBP phenotype was detected in most T cell leukemia cell lines, whereas the MICA ULBP phenotype characterized all acute myeloid leukemia and most B-cell lymphoma cell lines analyzed. These results, together with functional experiments, based on monoclonal antibody-mediated blocking of either NKG2D or its ligands, showed that killing of certain MICA cell tumors is at least in part NKG2D dependent. Indeed, leukemic T cells as well as certain B-cell lymphomas were killed in a NKG2D-dependent fashion upon recognition of ULBP molecules. Moreover, ULBP could induce NKG2D-mediated NK cell triggering also in tumors coexpressing MICA. Our data suggest that the involvement of NKG2D in natural killer cellmediated cytotoxicity strictly correlates with the expression and the surface density of MICA and ULBP on target cell tumors of different histotypes.
Time of Day Influences Nonattendance at Urgent Short-Term Mental Health Unit in Victoria, British Columbia

Objectives: To identify the patient profile of first-time no-shows (FTNS) and to examine which process variables predict FTNS. Method: We developed a questionnaire exploring variables that might impact attendance. Of 779 referrals over 9 months, all FTNS (n = 60) and a sample of randomly selected control subjects (n = 60) completed the questionnaire. Results: The FTNS rate was 7.7%. A set of 10 variables predicted FTNS at 80% accuracy. Most significant was our finding that “time of day of first appointment” showed a novel and practical difference between FTNS and control subjects. Patients were 3.6 times more likely to show for first appointments scheduled in the afternoon. Conclusions: Simply making first appointments in the afternoon could significantly decrease FTNS incidence.