Miracle-dz/UniFAR-FTUs huggingface dataset:
Influence of apoptosis (BCL2, FAS), Cell cycle (CCND1) and growth factor (EGF, EGFR) genetic polymorphisms on survival outcome: An exploratory study in squamous cell esophageal cancer

The study aimed at investigating whether genetic polymorphisms in BCL2, FAS, CCND1, EGF and EGFR genes influence the outcome of patients of esophageal squamous cell cancer treated with radiotherapy, with or without chemotherapy. Sixty nine histologically confirmed, previously untreated, patients with a squamous cell esophageal cancer were inducted into this study. Genotyping of BCL2 (ala43thr), FAS (A-670G), CCND1 (G870A), EGF (+61A/G) and EGFR (G497A) polymorphisms were determined using the polymerase chain reaction followed by restriction fragment length polymorphism methodology. Genotyped data was analyzed using univariate and multivariate logistic regression statistical tests for predicting the survival outcome. Genotypes of BCL2, FAS, CCND1 and EGFR polymorphisms independently did not influence outcome significantly. However, patients with EGF +61AG genotype had median survival of 25.5 months [95% CI = 5.2–45.5], whereas those with EGF +61GG genotype had survival of only 3.7 months [95% CI = 0.0–9.8, P=0.006]. In univariate cox-regression analysis, interaction of genotypes EGF+61GG*radiotherapy tumor dose (≤50 Gy) and EGF+61GG*upper third tumor location showed high hazard of death, 6.6 [95%CI = 2.0-21.5, P=0.002] and 26.8 [95%CI=3.7-194.2, P=0.001] while EGF+61AG*middle third tumor location had reduced hazard 0.20 [95%CI=0.06-0.60, P=0.004]. The pilot study suggests that EGF +61AG and +61GG genotypes may predict clinical outcome in esophageal cancer patients treated with radiotherapy with or without chemotherapy. EGF +61AG genotype was associated with improved survival, however +61GG genotype adversely affected the outcome in patients particularly with upper third location of tumor and lower dose (≤50) of radiotherapy.
Large and unexpected enrichment in stratospheric 16O13C18O and its meridional variation

The stratospheric CO2 oxygen isotope budget is thought to be governed primarily by the O(1D)+CO2 isotope exchange reaction. However, there is increasing evidence that other important physical processes may be occurring that standard isotopic tools have been unable to identify. Measuring the distribution of the exceedingly rare CO2 isotopologue 16O13C18O, in concert with 18O and 17O abundances, provides sensitivities to these additional processes and, thus, is a valuable test of current models. We identify a large and unexpected meridional variation in stratospheric 16O13C18O, observed as proportions in the polar vortex that are higher than in any naturally derived CO2 sample to date. We show, through photochemical experiments, that lower 16O13C18O proportions observed in the midlatitudes are determined primarily by the O(1D)+CO2 isotope exchange reaction, which promotes a stochastic isotopologue distribution. In contrast, higher 16O13C18O proportions in the polar vortex show correlations with long-lived stratospheric tracer and bulk isotope abundances opposite to those observed at midlatitudes and, thus, opposite to those easily explained by O(1D)+CO2. We believe the most plausible explanation for this meridional variation is either an unrecognized isotopic fractionation associated with the mesospheric photochemistry of CO2 or temperature-dependent isotopic exchange on polar stratospheric clouds. Unraveling the ultimate source of stratospheric 16O13C18O enrichments may impose additional isotopic constraints on biosphere–atmosphere carbon exchange, biosphere productivity, and their respective responses to climate change.
Arsenic trioxide preferentially induces nonapoptotic cell deaths as well as actin cytoskeleton rearrangement in the CHO AA8 cell line.

INTRODUCTION The therapeutic effect of arsenic trioxide (ATO, As2O3) has been investigated for many years. However, the precise molecular mechanisms underlying the antitumor activity of ATO are still not fully understood, but seem to depend on cell types, dosage, and duration of exposure. The purpose of this study was to assess the actin cytoskeleton rearrangement during the cell death process induced by arsenic trioxide in the CHO AA8 cells. A better understanding the mechanisms of ATO-action is likely to lead to more rational use of this drug either as monotherapies or in combination with other anticancer agents. MATERIAL AND METHODS The effect of ATO on actin cytoskeleton was studied in Chinese Hamster Ovary AA8 cell line. Actin was visualized by fluorescence microscopy and phalloidin conjugated to Alexa Fluor® 488. Morphological and ultrastructural alterations in the CHO AA8 cells were evaluated by using light and electron microscope, respectively. For quantitative measurement of cell death, Annexin V-Alexa Fluor® 488 and Propidium Iodide assay was performed. The vital staining of CHO AA8 cells with acridine orange was applied to detect the development of acidic vesicular organelles (AVOs). RESULTS The performed experiments revealed a dose-dependent decrease in the cell survival. The morphological and ultrastructural features acquired by the cells after ATO-treatment were considered as typical for autophagy and mitotic cell death. As was shown by acridine orange staining, arsenic trioxide treatment increased red fluorescence signals in dose-dependent manner, indicating the development of AVOs, a hallmark of autophagy. Low level of apoptosis was induced in the ATO-treated CHO AA8 cells. Furthermore, the rearrangement of actin filaments associated with cell death process was also detected. CONCLUSIONS The obtained results suggest that arsenic trioxide preferentially induces nonapoptotic cell deaths, autophagy and mitotic cell death, in p53-deficient CHO AA8 cells. Furthermore, the distinctive patterns of F-actin remodeling after As2O3 treatment were associated with different modes of cell death, confirming that cytoskeleton is a dynamic structure actively involved in the cell death process.
Clinical study of arterial anatomic variations for transradial coronary procedure in Chinese population.

BACKGROUND The radial artery is currently regarded as a useful approach for coronary intervention procedures. Adequate anatomical information of the radial artery should be helpful in performing transradial coronary procedures. Few data about the Chinese population have been obtained in this field. Therefore, we tried to evaluate the incidence and clinical significance of anomalous patterns, and their influence on the intervention procedure. METHODS In an estimated sample of 3000 cases, radial artery and subclavical artery angiography were performed after insertion of the sheath and coronary angiography (CA). The evaluable data including branch anomaly, tortuosity of the radial artery and procedural characteristics were analyzed. The procedure success was defined as CA or percutaneous coronary intervention (PCI) completed with the initial radial artery approach without changing to other routes. RESULTS In this study, 1897 cases of CA was undertaken and 1103 cases of CA combined with PCI were performed. The success rate of transradial intervention (TRI) was 96.6% (2899/3000). The approach in 44 cases was changed to the contralateral radial artery and 57 cases were changed to the brachial artery or femoral artery due to failure with the initial radial artery approach. The angiography of the upper limb artery was performed in all cases. Anatomic variations of upper limb arteries were noted in 610 patients (20.3%), which included tortuous configurations of the radial artery (5.0%), hypoplasias (2.2%), radioulnar loop (1.1%), abnormal origin of the radial artery (7.7%), stenosis of radial artery (1.4%), a tortuous configuration of the brachial artery (0.9%), a tortuous configurations of the subclavian artery (1.9%), lusoria subclavian artery (0.1%), and subclavian artery occlusion (0.03%). The procedural success rate in the normal population was higher than in the variation group (97.6% vs 93.0%, P < 0.001). In addition, other procedural outcomes and incidence of complications except radial artery occlusion were also significantly superior to variation group. CONCLUSIONS Anatomic variations of the radial artery were common, making up an important limitation in the trans-radial approach. Selection of appropriate instruments and understanding some tips and tricks were helpful to overcome the obstacles and effectively reduce the learning curve.
Endothelin‐1 exacerbates lipid accumulation by increasing the protein degradation of the ATP‐binding cassette transporter G1 in macrophages

Endothelin‐1 (ET‐1), a potent proatherogenic vasoconstrictive peptide, is known to promote macrophage foam cell formation via mechanisms that are not fully understood. Excessive lipid accumulation in macrophages is a major hallmark during the early stages of atherosclerotic lesions. Cholesterol homeostasis is tightly regulated by scavenger receptors (SRs) and ATP‐binding cassette (ABC) transporters during the transformation of macrophage foam cells. The aim of this study was to investigate the possible mechanisms by which ET‐1 affects lipid accumulation in macrophages. Our results demonstrate that oxidized low‐density lipoprotein (oxLDL) treatment increases lipid accumulation in rat bone marrow‐derived macrophages. Combined treatment with ET‐1 and oxLDL significantly exacerbated lipid accumulation in macrophages as compared to treatment with oxLDL alone. The results of Western blotting show that ET‐1 markedly decreased the ABCG1 levels via ET type A and B receptors and activation of the phosphatidylinositol 3‐kinase pathway; however, ET‐1 had no effect on the protein expression of CD36, SR‐BI, SR‐A, or ABCA1. In addition, real‐time PCR analysis showed that ET‐1 treatment did not affect ABCG1 mRNA expression. We also found that ET‐1 decreases ABCG1 possibly due to the enhancement of the proteosome/calpain pathway‐dependent degradation of ABCG1. Moreover, ET‐1 significantly reduced the efficiency of the cholesterol efflux in macrophages. Taken together, these findings suggest that ET‐1 may impair cholesterol efflux and further exacerbate lipid accumulation during the transformation of macrophage foam cells. J. Cell. Physiol. 226: 2198–2205, 2011. © 2010 Wiley‐Liss, Inc.
Suppression of Gluconeogenesis After a 3-Day Fast Does Not Deplete Liver Glycogen in Patients With NIDDM

To determine the effect of inhibition of gluconeogenesis on liver glycogen stores in patients with non-insulin-dependent diabetes mellitus (NIDDM) after a 3-day fast, 10% ethanol (EtOH) was administered intravenously to nine obese patients with NIDDM and six obese nondiabetic subjects. Rates of glucose appearance (3-[3H]glucose) and [U-14C]alanine incorporation into glucose (alanine gluconeogenesis [Ala-GNG]) were determined before and during EtOH administration, and residual glycogen stores were assessed by the incremental glucose response to glucagon (glucoseAUC). Hepatic glucose output (HGO) was closely correlated with plasma glucose levels (r = 0.71, P < 0.001) after the 3-day fast and was significantly greater in the diabetic compared with the nondiabetic subjects (13.8 ± 1.4 vs. 7.6 ± 0.6 μmol · kg−1 FFM · min−1 P < 0.01). During the 120-min EtOH infusion, Ala-GNG fell by more than 50% in both groups and did not increase after intravenous glucagon administration. HGO fell modestly in both the diabetic and nondiabetic subjects during the first 30 min of EtOH infusion and stabilized thereafter. In contrast to Ala-GNG, HGO increased significantly after intravenous glucagon administration in both the diabetic and nondiabetic subjects, but the increase was significantly greater in the patients with NIDDM (P < 0.01). The glucose area under the curve in response to glucagon (glucoseAUC) was lower in the presence of EtOH than in its absence (14.9 ± 7 vs. 68 ± 15.6 mM/min, P < 0.01) in the obese nondiabetic subjects, which suggests a decrease in liver glycogen stores. In contrast, EtOH infusion did not alter the glucoseAUC in obese diabetic subjects compared with saline control studies (134.7 ± 17.8 vs. 102.6 ± 20 mM/min, NS). The persistent increase in glucoseAUC suggests that glycogen stores are not depleted by EtOH-induced suppression of gluconeogenesis in patients with NIDDM after a 3-day fast.
Evaluation of Toxicity of Commercial Ophthalmic Fluoroquinolone Antibiotics as Assessed on Immortalized Corneal and Conjunctival Epithelial Cells

Purpose: To evaluate the toxicity of a variety of the fluoroquinolone antibiotics on the ocular surface by using tissue culture models of corneal epithelial cells and conjunctival epithelial cells. Methods: Immortalized conjunctival (CCC) and human corneal (HCE) epithelial cells were grown and when confluent the cells allowed to air dry for 1 hour. Medium was then replaced with 100 μL of one of the following: 1) Vigamox [moxifloxacin (0.5%: MX)]; (2) Zymar [gatifloxacin (0.3%: GA)]; 3) Quixin [levofloxacin (0.5%: LE)]; 4) Ocuflox [ofloxacin (0.3%: OF)]; 5) Ciloxan [ciprofloxacin (0.3%: CP)]; 6) medium (viable control); 7) “normal”/physiologic saline; 8) formalin (dead control). After one hour, 150 μL of MTT (3--[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazonium bromide was added and incubated for 4 hours. After decanting, precipitate was dissolved in 150 μL of isopropanol. Absorbance was determined at 572 nm. Results: The lowest amount of cell death was associated with the viable control. All ophthalmic preparations showed both corneal and conjunctival cell toxicity. Aside from the viable control, normal saline showed the next lowest amount of toxicity. Of the topical ocular antibiotics tested, MX showed the least amount of toxicity. All of the other antibiotics tested were statistically indistinguishable from each other. Conclusions: All of the topical ocular antibiotics tested showed evidence of both corneal and conjunctival toxicity (MX < OF ≤ LE ≤ CP ≤ GA), although only MX was statistically significant. Whether this finding reflects on in vivo wound healing remains to be determined. This model provides a rapid and cost-effective method to screen for surface toxicity of topical agents.
Correlation of C3 level with severity of generalized myasthenia gravis

Acute exacerbation of generalized myasthenia gravis (GMG) can cause swallowing impairment, respiratory failure, or death. It is important to identify immunological factors that might be regarded reliably as an index of the patient's clinical condition, response to treatment, and measure of certain immune aberrations of MG. In this study we investigated correlations between complement component C3, acetylcholine receptor antibody (AChRab) titer, and clinical severity of GMG. AChRab titer and C3 concentration were determined by radioimmunoassay and nephelometry, respectively. The clinical severity of GMG was assessed by the quantitative MG score (QMGS) according to Besinger and colleagues. Our findings indicate that the C3 level correlates with clinical severity of AChRab‐positive GMG. Muscle Nerve, 2009
How Banks' Strategies Infuence Financial Cycles: An Approach to Identifying Micro Behavior

In this paper, we show that the values of parameters of a well-calibrated model are useful in detecting micro behavior. We use a calibration procedure suitable for validating agent-based models to show how the evolution of model parameters, obtained via a rolling window estimation, illustrates the evolution of agents’ strategies in response to different economic conditions. In this regard, we calibrate the well-known financial model of Brock and Hommes using three banking indices (i.e., the S&P SmallCap 600 Financials Index, the STOXX Europe 600 Banks, and the STOXX Asia/Pacific 600 Banks) running from 1994 to 2016. The choice of a spatially and temporally diversified dataset allows us to analyze differences and similarities in the behavior of banks belonging to the different macro areas, as well as to capture agents’ reaction to the several economic phases characterizing the time series investigated.
Association between cellular-telephone calls and motor vehicle collisions.

BACKGROUND Because of a belief that the use of cellular telephones while driving may cause collisions, several countries have restricted their use in motor vehicles, and others are considering such regulations. We used an epidemiologic method, the case-crossover design, to study whether using a cellular telephone while driving increases the risk of a motor vehicle collision. METHODS We studied 699 drivers who had cellular telephones and who were involved in motor vehicle collisions resulting in substantial property damage but no personal injury. Each person's cellular-telephone calls on the day of the collision and during the previous week were analyzed through the use of detailed billing records. RESULTS A total of 26,798 cellular-telephone calls were made during the 14-month study period. The risk of a collision when using a cellular telephone was four times higher than the risk when a cellular telephone was not being used (relative risk, 4.3; 95 percent confidence interval, 3.0 to 6.5). The relative risk was similar for drivers who differed in personal characteristics such as age and driving experience; calls close to the time of the collision were particularly hazardous (relative risk, 4.8 for calls placed within 5 minutes of the accident, as compared with 1.3 for calls placed more than 15 minutes before the accident; P<0.001); and units that allowed the hands to be free (relative risk, 5.9) offered no safety advantage over hand-held units (relative risk, 3.9; P not significant). Thirty-nine percent of the drivers called emergency services after the collision, suggesting that having a cellular telephone may have had advantages in the aftermath of an event. CONCLUSIONS The use of cellular telephones in motor vehicles is associated with a quadrupling of the risk of a collision during the brief time interval involving a call. Decisions about regulation of such telephones, however, need to take into account the benefits of the technology and the role of individual responsibility.
The Leading Causes and Consequences of Citizenship Pressure in the Hotel Industry

Purpose This study aims to examine the causes of citizenship pressure and to investigate the relationship between citizenship pressure, job stress and turnover intentions. Specifically, the current study examines the effects of the personality trait of neuroticism and the organizational cultures of bureaucracy and the market. Design/methodology/approach Data were collected from 224 hotel employees in the People’s Republic of China using a self-administered survey questionnaire. The participants completed measures examining citizenship pressure, personality, organizational culture, job stress and intention to quit. Structural equation modeling was used to test the research hypotheses. Findings The results showed that employees who are more neurotic are more likely to experience citizenship pressure. Moreover, citizenship pressure was found to increase job stress and turnover intentions. However, a bureaucratic culture, which prizes stability, was found to reduce citizenship pressure. Practical implications This study presents factors that may influence hotel employees’ perceptions of citizenship pressure and reveals the negative consequences of such pressure. Thus, the study results contribute to a better understanding of citizenship pressure and can be used to develop guidelines to reduce citizenship pressure in work environments. Originality/value To the best of the authors’ knowledge, the current study is the first empirical study to examine the antecedents and consequences of citizenship pressure in the hotel industry. Moreover, previous citizenship pressure studies have mainly been conducted in a Western cultural context; it is unclear whether citizenship pressure can be similarly observed in China, where the nature and form of employment relationships differ significantly from those in Western countries.
Diffusion-weighted MR imaging of intracerebral masses: comparison with conventional MR imaging and histologic findings.

BACKGROUND AND PURPOSE The purposes of this study were to find the role of diffusion-weighted MR imaging in characterizing intracerebral masses and to find a correlation, if any, between the different parameters of diffusion-weighted imaging and histologic analysis of tumors. The usefulness of diffusion-weighted imaging and apparent diffusion coefficient (ADC) maps in tumor delineation was evaluated. Contrast with white matter and ADC values for tumor components with available histology were also evaluated. METHODS Twenty patients with clinical and routine MR imaging/CT evidence of intracerebral neoplasm were examined with routine MR imaging and echo-planar diffusion-weighted imaging. The routine MR imaging included at least the axial T2-weighted fast spin-echo and axial T1-weighted spin-echo sequences before and after contrast enhancement. The diffusion-weighted imaging included an echo-planar spin-echo sequence with three b values (0, 300, and 1200 s/mm(2)), sensitizing gradient in the z direction, and calculated ADC maps. The visual comparison of routine MR images with diffusion-weighted images for tumor delineation was performed as was the statistical analysis of quantitative diffusion-weighted imaging parameters with histologic evaluation. RESULTS For tumors, the diffusion-weighted images and ADC maps of gliomas were less useful than the T2-weighted spin-echo and contrast-enhanced T1-weighted spin-echo images in definition of tumor boundaries. Additionally, in six cases of gliomas, neither T2-weighted spin-echo nor diffusion-weighted images were able to show a boundary between tumor and edema, which was present on contrast-enhanced T1-weighted and/or perfusion echo-planar images. The ADC values of solid gliomas, metastases, and meningioma were in the same range. In two cases of lymphomas, there was a good contrast with white matter, with strongly reduced ADC values. For infection, the highest contrast on diffusion-weighted images and lowest ADC values were observed in association with inflammatory granuloma and abscess. CONCLUSION Contrary to the findings of previous studies, we found no clear advantage of diffusion-weighted echo-planar imaging in the evaluation of tumor extension. The contrast between gliomas, metastases, meningioma, and white matter was generally lower on diffusion-weighted images and ADC maps compared with conventional MR imaging. Unlike gliomas, the two cases of lymphomas showed hyperintense signal on diffusion-weighted images whereas the case of cerebral abscess showed the highest contrast on diffusion-weighted images with very low ADC values. Further study is required to find out whether this may be useful in the differentiation of gliomas and metastasis from lymphoma and abscess.