Miracle-dz/UniFAR-FTUs huggingface dataset:
Desflurane Improves the Recovery of the Evoked Postsynaptic Population Spike From CA1 Pyramidal Cells After Hypoxia in Rat Hippocampal Slices*

Desflurane is a volatile anesthetic that allows rapid induction and emergence, reduces cerebral metabolism, and enhances tissue perfusion. We studied the effect of treatment with 4%, 6%, and 12% desflurane on hypoxic neuronal damage by comparing the size of the postsynaptic evoked population spike recorded from the cornu ammonis 1 (CA1) pyramidal cell layer of rat hippocampal slices before and 2 hours after a hypoxic insult. When the tissue was treated with 6% desflurane before, during, and after 3.5 minutes of hypoxia, recovery was significantly better in slices exposed to desflurane (37% ± 9%) compared with untreated hypoxic slices (15% ± 5%). A lower (4%) or higher (12%) concentration of desflurane did not significantly improve recovery after 3.5 minutes of hypoxia. In the period before hypoxia, 12% and 6% desflurane significantly increased the latency and decreased the amplitude of the postsynaptic population spike; 4% desflurane had a similar but nonsignificant effect on latency and amplitude. We conclude that 6% desflurane, a clinically useful concentration (1 minimal alveolar concentration), improved the recovery of postsynaptic evoked responses in rat hippocampal slices after 3.5 minutes of hypoxia. In vivo studies must be conducted to assess the potential clinical significance of 6% desflurane's neuroprotective activity.
Correcting radial and perspective distortion by using face shape information

In this paper, we propose a new technique for compensating radial and perspective distortions of photos acquired with wide-angle lens by using facial features detected from the images without using predefined calibration patterns. The proposed algorithm utilizes a statistical facial feature model to recover radial distortion and the facial features are further used for adaptive cylindrical projection which will reduce perspective distortion near the image boundary. Our algorithm has several advantages over the traditional methods. First, traditional calibration patterns, like man-made straight buildings, chessboards, or calibration cubes, are not required in our method. Even though the radial distortion can be corrected by several conventional methods, most of them usually produce photos with larger perspective distortion for faces compared to our method. The system is composed of four components: offline training of the statistical facial feature model, feature point extraction from distorted faces, estimation of radial distortion parameters and compensation of radial distortion, and adaptive cylindrical projection. In order to estimate the distortion parameters, we propose an energy considering the fitness between the undistorted coordinates of the facial feature points extracted from the input distorted image and the learned statistical facial feature model. Given the distortion parameters, the fitness is calculated by solving a linear least squares system. The distortion parameters that minimize the cost function are searched in a hierarchical manner. Experimental results demonstrate the distortion reduction in the corrected images by using the proposed method.
Enhancing Macroautophagy Protects against Ischemia/Reperfusion Injury in Cardiac Myocytes*

Cardiac myocytes undergo programmed cell death as a result of ischemia/reperfusion (I/R). One feature of I/R injury is the increased presence of autophagosomes. However, to date it is not known whether macroautophagy functions as a protective pathway, contributes to programmed cell death, or is an irrelevant event during cardiac I/R injury. We employed simulated I/R of cardiac HL-1 cells as an in vitro model of I/R injury to the heart. To assess macroautophagy, we quantified autophagosome generation and degradation (autophagic flux), as determined by steady-state levels of autophagosomes in relation to lysosomal inhibitor-mediated accumulation of autophagosomes. We found that I/R impaired both formation and downstream lysosomal degradation of autophagosomes. Overexpression of Beclin1 enhanced autophagic flux following I/R and significantly reduced activation of pro-apoptotic Bax, whereas RNA interference knockdown of Beclin1 increased Bax activation. Bcl-2 and Bcl-xL were protective against I/R injury, and expression of a Beclin1 Bcl-2/-xL binding domain mutant resulted in decreased autophagic flux and did not protect against I/R injury. Overexpression of Atg5, a component of the autophagosomal machinery downstream of Beclin1, did not affect cellular injury, whereas expression of a dominant negative mutant of Atg5 increased cellular injury. These results demonstrate that autophagic flux is impaired at the level of both induction and degradation and that enhancing autophagy constitutes a powerful and previously uncharacterized protective mechanism against I/R injury to the heart cell.
Verapamil Inhibits Aspergillus Biofilm, but Antagonizes Voriconazole

The paucity of effective antifungals against Aspergillus and increasing resistance, the recognition of the importance of Aspergillus biofilm in several clinical settings, and reports of verapamil—a calcium channel blocker—efficacy against Candida biofilm and hyphal growth, and synergy with an azole antifungal in vitro, led to a study of verapamil ± voriconazole against Aspergillus. Broth macrodilution methodology was utilized for MIC (minimum inhibitory concentration) and MFC (minimum fungicidal concentration) determination. The metabolic effects (assessed by XTT [2,3-bis[2-methoxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxanilide inner salt]) on biofilm formation by conidia were studied upon exposure to verapamil, verapamil plus voriconazole, or voriconazole alone. For biofilm formation, we found less inhibition from the combinations than with either drug alone, or less inhibition from the combination than that of the more potent drug alone. For preformed biofilm, we found no significant change in activity comparing voriconazole alone compared to added verapamil, and no significant alteration of activity of the more potent voriconazole, at any concentration in the range tested, by addition of a concentration of verapamil that is inhibitory alone. In full checkerboard assays with planktonic fungus, there was no indication of any effect of one drug on the other (indifference). Although verapamil was similarly inactive against planktonic Aspergillus, as with Candida, verapamil was indeed active against Aspergillus biofilm. However, indifference and antagonism was found with voriconazole.
Basic fibroblast growth factor-binding peptide as a novel targeting ligand of drug carrier to tumor cells

Drug systems targeting tumor cells using basic fibroblast growth factor (bFGF) have been widely reported. In this study, the peptide KRTGQYKLC (bFGFp), containing cysteine at the carboxyl termination of the bFGF-derived peptide, was applied as a novel ligand targeting tumor cells. bFGFp was conjugated with bovine serum albumin (BSA) and liposomes. The peptide was shown to inhibit the binding of bFGF to FGF receptor-1 (FGFR1). Interestingly, the binding study using surface plasmon resonance (SPR) assay revealed that the bFGFp–BSA was not bound to FGFR1, but was selectively bound to bFGF. Furthermore, the SPR assay showed that bFGFp–BSA is capable of binding to FGFR1 following the pretreatment with bFGF. The confocal microscopy study indicated that the uptake of bFGFp–BSA by NIH3T3 cells, which highly express FGFRs, was significantly enhanced by pretreatment with bFGF. Then, PEGylated liposomes containing bFGFp (bFGFp–liposome) were prepared by conjugating maleimide-PEG-PE with bFGFp. Following the pretreatment of bFGF, the uptake of bFGFp–liposomes by NIH3T3 cells was significantly enhanced. These results suggest that bFGFp–BSA and bFGFp–liposomes are taken by NIH3T3 cells via binding with bFGF. In addition, both bFGFp–BSA and bFGFp–liposomes had no effect on the proliferation of NIH3T3 cells. This strategy can be used as a novel system for targeting tumors highly expressing FGFRs without a proliferation effect.
Longitudinal analysis on the effect of insertion torque on delayed single implants: A 3‐year randomized clinical study

BACKGROUND Implant stability is commonly related to insertion torque. Recently, it has been suggested that higher insertion torque may lead to greater bone resorption. PURPOSE The aim of the present randomized clinical study was to evaluate the role of different insertion torque values in terms of implant success, marginal bone loss, and facial soft tissues recession. MATERIALS AND METHODS Patients requiring a single dental implant were recruited and randomized to receive one of two implants with the same macro-geometry but different cutting designs. First group consists of a 90 degrees cutting groove know as self-tapping implant, and the second group known as Blossom™ cutting groove. (Intra-Lock, Boca Raton, Florida). The insertion torque (IT) was assessed and two groups followed: high-IT (≥50 Ncm) group and regular-IT (<50 Ncm) group. After 3 months, all the implants were restored. At baseline, buccal bone thickness (BBT) was recorded. During the 3-year survey, the following outcomes had been registered: implant failures and success, radiographic marginal bone level around dental implant (MBL) and facial soft tissue level (FSTL). RESULTS A hundred and sixteen implants were placed in healed sites. The overall survival rate after 3 years was 96.5%. The Cumulative Success Rate was 91.3% for the High IT group and 98.2% for the Regular IT group. The mean marginal bone loss and facial soft tissue recession, at a 3-year evaluation, were significantly greater for the High-IT group and in the mandible than that reached in the Regular-IT group and in the maxilla. CONCLUSION Present findings showed that implants placed with higher insertion torque in mandible led to greater bone resorption and mucosal recession than that registered for implants placed with a regular IT. Moreover, sites with a thick buccal bone wall (≥1 mm) showed smaller recession at the facial soft tissue level after 3 years.
The apolipoprotein e knockout mouse: a model documenting accelerated atherogenesis in uremia.

Rodents do not develop spontaneous atherosclerosis. Currently, there is no good animal model to study the effect of uremia on atherosclerosis. This study evaluated whether apolipoprotein E knockout (Apoe-/-) mice are useful to study the effect of renal dysfunction on cardiovascular risk. Apoe-/- mice have decreased serum apolipoprotein E and exhibit lipid abnormalities and atherosclerosis even on a low-cholesterol diet. Ten-wk-old Apoe-/- mice were subtotally nephrectomised (SNX Apoe-/-; n = 8), uninephrectomised (UNX Apoe-/-; n = 5), or sham-operated (sham Apoe-/-; n = 5) and compared with their genetic controls (SNX C57/BL6; UNX C57/BL6; sham C57/BL6). After 12 wk, BP was measured intraarterially, blood samples were taken, and the experiment was terminated by perfusion fixation. The heart weight was determined, and quantitative morphologic analysis of intramyocardial arteries and aortic changes was performed. At the end of the experiment, heart weight and relative left ventricular weight were comparable in all groups. Intraarterial BP was somewhat higher in Apoe-/- mice compared with controls. Baseline serum cholesterol and triglyceride levels were higher in Apoe-/- mice than in C57/BL6. Atherosclerotic plaques were not present in sham or UNX C57/BL6, but minor plaque formation was noted in some SNX control animals. In contrast, beginning plaques were seen even in untouched Apoe-/- mice, and strikingly increased plaque formation was noted in UNX and SNX Apoe-/- mice. Maximal plaque diameter (cross-section) was 37 +/- 74 micro m in SNX C57/BL6, 191 +/- 90 micro m in sham Apoe-/-, 323 +/- 66 micro m in UNX Apoe-/-, and 457 +/- 17 micro m in SNX Apoe-/-. The plaque morphology corresponded with that of early plaques characterized by foam cells and virtual absence of lymphocytes or smooth muscle cell infiltration. In conclusion, even mild renal dysfunction, i.e., after uninephrectomy, causes a dramatic increase in plaque size and aggressive morphology (foam cell rich soft plaques) in the animal model of the Apoe-/- mouse.
Progenitor/Stem Cell Markers in Brain Adjacent to Glioblastoma: GD3 Ganglioside and NG2 Proteoglycan Expression

Characterization of tissue surrounding glioblastoma (GBM) is a focus for translational research because tumor recurrence invariably occurs in this area. We investigated the expression of the progenitor/stem cell markers GD3 ganglioside and NG2 proteoglycan in GBM, peritumor tissue (brain adjacent to tumor, BAT) and cancer stem-like cells (CSCs) isolated from GBM (GCSCs) and BAT (PCSCs). GD3 and NG2 immunohistochemistry was performed in paired GBM and BAT specimens from 40 patients. Double-immunofluorescence was carried out to characterize NG2-positive cells of vessel walls. GD3 and NG2 expression was investigated in GCSCs and PCSCs whose tumorigenicity was also evaluated in Scid/bg mice. GD3 and NG2 expression was higher in tumor tissue than in BAT. NG2 decreased as the distance from tumor margin increased, regardless of the tumor cell presence, whereas GD3 correlated with neoplastic infiltration. In BAT, NG2 was coexpressed with &agr;-smooth muscle actin (&agr;-SMA) in pericytes and with nestin in the endothelium. Higher levels of NG2 mRNA and protein were found in GCSCs while GD3 synthase was expressed at similar levels in the 2 CSC populations. PCSCs had lower tumorigenicity than GCSCs. These data suggest the possible involvement of GD3 and NG2 in pre/pro-tumorigenic events occurring in the complex microenvironment of the tissue surrounding GBM.
Haplotype transmission disequilibrium and evidence for linkage of the CHRNA7 gene region to schizophrenia in Southern African Bantu families.

Recent reports have strongly linked markers near the alpha-7 nicotinic cholinergic receptor subunit gene on human chromosome 15q13-q14 to a sensory gating deficit common in schizophrenics, and have shown positive though non-significant results linking this region to the primary phenotype of schizophrenia in a sample of North American families. We therefore tested for linkage between markers in this region of chromosome 15q and schizophrenia in a sample of 15 multiply affected and 5 single case families with schizophrenia drawn from the Bantu-speaking black population of South Africa. An initial replication using markers from the original study gave an affected-only LOD score maximum of 1.08 under a recessive model at Theta=0.00 for D15S1360, a dinucleotide polymorphism found on the same YAC as the alpha-7 receptor gene. Nonparametric affected-only multipoint analysis gave a Z-score of 1. 29, P=0.098, for D15S1360, and Z=1.45, p=0.075 for D15S118. We then increased the resolution of the map with an extended set of 20 markers. Again, two peaks were observed, with NPL scores of 1.81, p=0.037, at D15S1043 and 1.79 at D15S1360 and 1.80 at D15S1010, both p=0.037. Transmission disequilibrium testing of data from D15S1360 gave an allele-wise and genotype-wise chi(2) of 6.59, 2 df, p=0.037. Haplotype transmission disequilibrium testing using a restricted allele and haplotype set from D15S1043 and D15S1360 gave a global chi(2) of 10.647, 4 df, P=0.007, and a maximum chi(2) of 6.567, 1 df, P=0.004 for excess transmission of the 1.2 haplotype into affected offspring. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:196-201, 2000.
The natural history of hepatitis C virus in pediatric liver transplant recipients

Although rare in the pediatric population, the natural history of hepatitis C virus (HCV) recurrence in pediatric patients undergoing orthotopic liver transplantation (OLT) for end‐stage liver disease secondary to HCV has not been well described. We performed an analysis of all 67 pediatric patients (<17 years old) who have undergone OLT for HCV in the United States between 1/1988 and 6/2005. The 67 pediatric patients received a total of 83 OLTs for HCV. Following initial OLTs performed for HCV, the patient and allograft survival rates were 71.6% and 55.0%, respectively, at 5 years. Following retransplantation these rates decreased to 55.0% and 33.8%, respectively, following retransplantation. Recipients were listed for retransplantation after 31.3% of all OLTs, and overall recipients were retransplanted after 19.3% of OLTs. The overwhelming majority of retransplants were performed for HCV recurrence. A mean of 1.2 OLTs were performed per patient for HCV. The median time between OLTs for HCV was 290 days. In conclusion, the risk of HCV recurrence in pediatric OLT recipients is high and is associated with a high rate of retransplantation. Still, OLT represents the only treatment option that may achieve long‐term survival in pediatric patients with end‐stage liver disease secondary to HCV that is recalcitrant to medical management. Liver Transpl 12:1119–1123, 2006. © 2006 AASLD.
Pacing From the Right Ventricular Septum and Development of New Atrial Fibrillation in Paced Patients With Atrioventricular Block and Preserved Left Ventricular Function.

BACKGROUND Whether pacing from the right ventricular (RV) septum improves prognosis is unclear. Furthermore, the clinical characteristics of patients who develop atrial fibrillation (AF) and cardiovascular events during long-term RV septal pacing have not been described.Methods and Results:We retrospectively evaluated the incidence of AF and cardiovascular events, including cardiac death, heart failure requiring hospitalization, or stroke, for a median of 4.0 years in 123 recipients of dual-chamber pacemakers implanted for atrioventricular block with preserved left ventricular function, who were free from AF before device implantation. AF developed in 30 patients (24%), and multivariable analysis suggested that the cumulative percentage of RV pacing was the only independent predictor of newly developed AF (hazard ratio: 1.19 for each 10% increment; 95% confidence interval: 1.04-1.41; P=0.01). Furthermore, older age, newly developed AF and a paced QRS duration ≥155 ms at pacemaker implantation were significant predictors of cardiovascular events. CONCLUSIONS RV septum pacing may induce AF in up to one-quarter of patients paced for atrioventricular block, according to the frequency of pacing. More importantly, in such patients, AF induced by RV pacing and a paced QRS duration ≥155 ms at pacemaker implantation are significantly associated with poor prognosis. Therefore, we recommend pacing from sites producing a paced QRS duration <155 ms and avoiding unnecessary RV pacing. (Circ J 2016; 80: 2302-2309).
Chloride Efflux is Involved in ET-1 and 5-HT-Induced Contraction in Rabbit Basilar Artery

Chloride (Cl−) efflux induces depolarization and contributes to contraction of cerebral arteries. We tested the effect of endothelin-1 and 5-hydroxytryptamine on isometric tension in rabbit basilar artery by inhibition of Na+-K+-2Cl− co-transporter and Cl−/HCO3− exchanger to decrease Cl−, by decreasing extracellular Cl− concentration, and by blocking Cl− channels using Cl− channel inhibitors. We have made the following observations: (i) endothelin-1 and 5-hydroxytryptamine produced contraction in the normal Cl− Krebs-Henseleit bicarbonate solution (123 mM Cl−); (ii) inhibition of Na+-K+-2Cl− co-transporter with bumetanide abolished the contractions; (iii) bicarbonate-free solution with HEPES reduced contractions to 5-hydroxytryptamine and endothelin-1; (iv) substitution of extracellular Cl− with methanesulfonate acid (MS- 113 mM, Cl− 10 mM) enhanced peak contraction to 5-hydroxytryptamine and endothelin-1 and decreased plateau contraction to 5-hydroxytryptamine, but did not affect the plateau contraction to endothelin-1 and KCl; and (v) blockade of Ca2+-dependent Cl− channel with niflumic acid and non-selective Cl− channel with 5-nitro-2-(3-phenylpropylamino) benzoic acid and indanyloxyacetic acid-94, R- (+)-methylindazone (R- (+)-IAA-94) decreased contractions to endothelin-1 and 5-hydroxytryptamine. However, removal of endothelium attenuated the effect of Cl− channel inhibitors. In conclusion, Cl− channels and Cl− flux are involved in endothelin-1-induced and 5-hydroxytryptamine-induced contraction in rabbit basilar artery. Cl− channel blockers might exert additional effects by releasing vasodilatation agents from endothelial cells.
NADPH oxidases in vascular pathology.

SIGNIFICANCE Reactive oxygen species (ROS) play a critical role in vascular disease. While there are many possible sources of ROS, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases play a central role. They are a source of "kindling radicals," which affect other enzymes, such as nitric oxide synthase endothelial nitric oxide synthase or xanthine oxidase. This is important, as risk factors for atherosclerosis (hypertension, diabetes, hypercholesterolemia, and smoking) regulate the expression and activity of NADPH oxidases in the vessel wall. RECENT ADVANCES There are seven isoforms in mammals: Nox1, Nox2, Nox3, Nox4, Nox5, Duox1 and Duox2. Nox1, Nox2, Nox4, and Nox5 are expressed in endothelium, vascular smooth muscle cells, fibroblasts, or perivascular adipocytes. Other homologues have not been found or are expressed at very low levels; their roles have not been established. Nox1/Nox2 promote the development of endothelial dysfunction, hypertension, and inflammation. Nox4 may have a role in protecting the vasculature during stress; however, when its activity is increased, it may be detrimental. Calcium-dependent Nox5 has been implicated in oxidative damage in human atherosclerosis. CRITICAL ISSUES NADPH oxidase-derived ROS play a role in vascular pathology as well as in the maintenance of normal physiological vascular function. We also discuss recently elucidated mechanisms such as the role of NADPH oxidases in vascular protection, vascular inflammation, pulmonary hypertension, tumor angiogenesis, and central nervous system regulation of vascular function and hypertension. FUTURE DIRECTIONS Understanding the role of individual oxidases and interactions between homologues in vascular disease is critical for efficient pharmacological regulation of vascular NADPH oxidases in both the laboratory and clinical practice.
Apport de la simulation dans l'analyse de stratégies de maintenance

On se propose, dans ce papier, d'explorer le potentiel de la simulation dans le processus de developpement de nouvelles strategies de maintenance d'equipements dont les caracteristiques operatoires se degradent avec l'usage et dont les durees de vie et de reparation sont aleatoires. Pour ce, nous presentons le langage de simulation RAO et nous illustrons son potentiel via des exemples de strategies de maintenance. RAO (Ressource Action Operation ) est un simulateur a evenements discrets. Cet outil propose une tres grande souplesse de modelisation, permet de suivre l'evolution de chaque ressources et offre des possibilites d'animation.