Miracle-dz/UniFAR-FTUs huggingface dataset:
Calmodulin mRNA in Barley (Hordeum vulgare L.) : Apparent Regulation by Cell Proliferation and Light.

Calmodulin is encoded by a 650-nucleotide mRNA in higher plants. This messenger was identified in barley and pea by a combination of in vitro translation and blot hybridization experiments using anti-sense RNA produced from an eel calmodulin cDNA probe. In all plant tissues tested, calmodulin mRNA represents between 0.01 and 0.1% of the total translatable mRNA population. Calmodulin mRNA levels are three- to fourfold higher in the meristematic zone of the first leaf of barley. At all other stages of leaf cell differentiation, calmodulin mRNA levels are nearly identical. During light-induced development in barley leaves, the relative proportion of translatable calmodulin mRNA declines about twofold. Cytoplasmic mRNAs that may encode calmodulin-like proteins were also detected. The levels of several of these putative Ca(2+)-binding protein mRNAs are modulated during the course of light-induced barley leaf cell development.
Oil Price Shocks and Inflation in Iran: Quantile Regression Approach

Iran's economy, like most other oil-exporting countries is extremely vulnerable to oil price fluctuations. Due to the high share of oil sector in GDP, oil price fluctuations can destabilize the economy leading to high inflations. In this study based on the annual data for the period of 19822015 and using quantile regression method, inflation as the dependent variable is regressed on oil prices, GDP, liquidity and trade openness. According to the results, there is a positive relationship between inflation and oil price fluctuations in different deciles. The effect of GDP and trade openness on inflation is negative and the effect of liquidity is positive
Near real-time SAR change detection using CUDA

In this paper, near real-time GPU implementations of two efficient SAR change detection methods using closed-form Kullback-Leibler divergence between generalized Gamma distributions (KL-GGD) and two densities approximated by Edgeworth series (KL-EW) are investigated and compared in terms of both accuracy and speed. The near real-time implementations of the proposed methods using Compute Unified Device Architecture (CUDA) on Graphics Processing Units (GPUs) are described and evaluated. The computation time of the parallel implementation on GPU is compared with the C/C++ implementation on Central Processing Unit (CPU). Our experimental results show that the GPU implementation is at least twenty times faster than the CPU implementation.
Does inflammation influence atrial fibrillation recurrence following catheter ablation?

Recent clinical and experimental data suggest the pivotal role of inflammation in the pathogenesis of atrial fibrillation (AF). Large epidemiological studies have linked an amplified baseline inflammatory state with the development of cardiovascular events, including future AF,1 whereas certain inflammatory cytokines have been used to predict AF recurrence following successful electrical or chemical cardioversion.2,3 The increased incidence of AF following cardiac surgery, which is known to induce a potent inflammatory response through ischaemia, cardiopulmonary bypass, and cardiotomy, has further implicated inflammation in the pathogenesis of AF.4 In addition, patients with documented AF have demonstrated features of chronic inflammation that is proportional to the type and chronicity of AF.5 Finally, medications with an established anti-inflammatory effect, such as statins and corticosteroids, have been successfully used for primary and secondary prevention of AF.6,7 Despite occasional methodological limitations or heterogeneity between clinical and experimental studies, the association between inflammation and AF is apparent. However, the exact mechanisms by which inflammation causes the initiation or perpetuation of the arrhythmia can only be speculated. Conditions that predispose to oxidative stress, ischaemia, and ultimately tissue injury lead to the release of acute phase proteins and disarray of cellular membranes. Spatial derangement of the phospholipid bilayer under enzymatic interaction with secretory phospholipase A2 generates lysophosphatidylcholine, which is a ligand for C-reactive protein.8 The binding of C-reactive protein to lysophospholipids activates the complement cascade, neutrophil influx, and phagocytosis. This process may not accurately distinguish between irreversibly … *Corresponding author. Tel: +44 2087252652. Email: akou{at}doctors.org. uk
Dilated intercellular spaces: a morphological feature of acid reflux--damaged human esophageal epithelium.

BACKGROUND & AIMS Dilated intercellular spaces are a sign of epithelial damage in acid-perfused rabbit esophagus, a change best identified by transmission electron microscopy. The aim of this study was to determine if this change is also a feature of acid damage to human esophageal epithelium. METHODS Endoscopic esophageal biopsy specimens from patients with (n = 11) and without (n = 13) recurrent heartburn were examined using transmission electron microscopy. Of 11 patients with heartburn, 6 had erosive esophagitis and 5 had normal-appearing mucosa on endoscopy; 13 controls had no symptoms or signs of esophageal disease. Using a computer, intercellular space diameter was measured from transmission electron microscopy photomicrographs of the specimen from each patient. RESULTS Intercellular space diameter was significantly greater in specimens from patients with heartburn than those from controls; this was true irrespective of whether the patient had erosive or nonerosive disease. Space diameters of > or = 2.4 microns were present in 8 of 11 patients with heartburn and in no controls. CONCLUSIONS Dilated intercellular spaces are a feature of reflux damage to human esophageal epithelium. As a morphological marker of increased paracellular permeability, its presence in patients without endoscopic abnormalities may help explain their development of heartburn.
Requirement of MIR165A primary transcript sequence for its activity pattern in Arabidopsis leaf primordia

miRNAs might move cell to cell and act as mobile signals in plant development, while the regulatory mechanisms of miRNA cell-to-cell movement are still unclear. Recently, in Arabidopsis leaf primordia, we revealed that miR165 from the MIR165A gene, which is expressed in the abaxial epidermal cells of leaf primordia, acts non-cell-autonomously in inner cells on the abaxial side. We proposed that not only mature miR165 sequence but also the MIR165A primary transcript sequence are required for the confinement of miR165 activity to the abaxial side of leaf primordia. The deletion analysis of the MIR165A genomic fragment showed that with a lack of the 3' region of MIR165A its activity is not confined in leaf primordia, suggesting that the full-length primary transcript of MIR165A is important for the regulatory mechanism of miRNA activity confinement in leaf primordia. It has been reported that the MIR165A transcript is predicted to be translated into the short poly peptide, proposing that the MIR165A transcript may be exported to the cytoplasm. Considering these matters, we propose a hypothesis for the confinement of miR165 activity to the abaxial side in leaf primordia dependent on the MIR165A primary transcript.
Intracellular Bax Translocation after Transient Cerebral Ischemia: Implications for a Role of the Mitochondrial Apoptotic Signaling Pathway in Ischemic Neuronal Death

Activation of terminal caspases such as caspase-3 plays an important role in the execution of neuronal cell death after transient cerebral ischemia. Although the precise mechanism by which terminal caspases are activated in ischemic neurons remains elusive, recent studies have postulated that the mitochondrial cell death-signaling pathway may participate in this process. The bcl-2 family member protein Bax is a potent proapoptotic molecule that, on translocation from cytosol to mitochondria, triggers the activation of terminal caspases by increasing mitochondrial membrane permeability and resulting in the release of apoptosis-promoting factors, including cytochrome c. In the present study, the role of intracellular Bax translocation in ischemic brain injury was investigated in a rat model of transient focal ischemia (30 minutes) and reperfusion (1 to 72 hours). Immunochemical studies revealed that transient ischemia induced a rapid translocation of Bax from cytosol to mitochondria in caudate neurons, with a temporal profile and regional distribution coinciding with the mitochondrial release of cytochrome c and caspase-9. Further, in postischemic caudate putamen in vivo and in isolated brain mitochondria in vitro, the authors found enhanced heterodimerization between Bax and the mitochondrial membrane permeabilization-related proteins adenine nucleotide translocator (ANT) and voltage-dependent anion channel. The ANT inhibitor bongkrekic acid prevented Bax and ANT interactions and inhibited Bax-triggered caspase-9 release from isolated brain mitochondria in vitro. Bongkrekic acid also offered significant neuroprotection against ischemia-induced caspase-3 and caspase-9 activation and cell death in the brain. These results strongly suggest that the Bax-mediated mitochondrial apoptotic signaling pathway may play an important role in ischemic neuronal injury.
Amplification of HER-2 in gastric carcinoma: association with Topoisomerase IIalpha gene amplification, intestinal type, poor prognosis and sensitivity to trastuzumab.

BACKGROUND HER-2/neu gene amplification has predictive value in breast cancer patients responding to trastuzumab. We wanted to investigate the frequency and clinical significance of HER-2/neu amplification in gastric carcinoma. PATIENTS AND METHODS The frequency of HER-2/neu and Topoisomerase IIalpha gene amplification was studied in adenocarcinomas of the stomach (n=131) and the gastroesophageal junction (n=100) by chromogenic in situ hybridization (CISH). Sensitivity of a gastric cancer cell line N87 with HER-2/neu amplification to trastuzumab was studied by a cell viability assay and compared with that of a HER-2 amplified breast cancer cell line SKBR-3. Growth inhibition of N87 cells was also verified in vivo in N87 xenograft tumors. RESULTS HER-2/neu amplification was present in 16 (12.2%) of the 131 gastric and in 24 (24.0%) of the 100 gastroesophageal adenocarcinomas. Co-amplification of Topoisomerase IIalpha was present in the majority of gastric (63%) and esophagogastric junction cancers (68%) with HER-2/neu amplification. HER-2/neu amplification was more common in the intestinal histologic type of gastric cancer (21.5%) than in the diffuse (2%) or the mixed/anaplastic type (5%, P=0.0051), but it was not associated with gender, age at diagnosis or clinical stage. Presence of HER-2/neu amplification was associated with poor carcinoma-specific survival (P=0.0089). HER-2/neu targeting antibody trastuzumab inhibited the growth of a p185(HER-2/neu) overexpressing gastric and breast carcinoma cell lines (N87 and SKBR-3) with equal efficacy. CONCLUSIONS HER-2/neu amplification is common in the intestinal type of gastric carcinoma, and it is associated with a poor outcome. HER-2 might be a useful target in this disease, and this hypothesis deserves to be investigated in clinical trials.
Filamentous growth of Candida albicans in response to physical environmental cues and its regulation by the unique CZF1 gene

Hyphal growth in the opportunistic fungal pathogen Candida albicans is believed to contribute to the virulence of the organism by promoting penetration of fungal cells into host tissue. In this study, stimulation of hyphal growth by a feature of the physical environment was demonstrated. Specifically, growth of cells embedded within a matrix promoted the formation of hyphae. The CZF1 gene, encoding a putative transcription factor, was shown to be involved in the regulation of hyphal growth under certain conditions, including embedded conditions. Ectopic expression of CZF1 in embedded cells promoted the rapid formation of hyphae. Elimination of CZF1 and CPH1, encoding a homologue of the Saccharomyces cerevisiae Ste12p transcription factor, led to a pronounced defect in filamentous growth of embedded cells. Elimination of CZF1 alone led to a moderate defect in hyphal growth under some conditions, including embedded conditions. Hyphal morphogenesis in response to matrix embedding may occur in the opportunistic pathogen, C. albicans, to promote invasion of fungal cells into host tissue.
On the social properties of mobility models: A genetic algorithm-based approach

The performance of routing protocols in MANETs is significantly influenced by the mobility of wireless devices. Recently, many social based mobility models generate synthetic traces to capture the statistical properties detected from real traces, leaving the cause of these movement patterns untouched. As a highlighted novelty of this paper, we explore the driving force of complicated social behaviors from an evolutionary point of view and propose a genetic algorithm-based mobility model (GAMM). Using “less movement cost, more social gains” as the metric of trace's fitness to the environment, Levy Walk and inter-contact time with truncated power-law distribution emerge from generations of evolutions, accompanied by the reduction of location entropy. Two practical extension models and a simulation experiment are also presented to show the expandability and scalability of GAMM.
Rapid temporal changes in the expression of a set of neuromodulatory genes during alcohol withdrawal in the dorsal vagal complex: molecular evidence of homeostatic disturbance.

BACKGROUND Chronic alcohol exposure produces neuroadaptation, which increases the risk of cellular excitotoxicity and autonomic dysfunction during withdrawal. The temporal progression and regulation of the gene expression that contributes to this physiologic and behavioral phenotype is poorly understood early in the withdrawal period. Further, it is unexplored in the dorsal vagal complex (DVC), a brainstem autonomic regulatory structure. METHODS We use a quantitative polymerase chain reaction platform to precisely and simultaneously measure the expression of 145 neuromodulatory genes in more than 100 rat DVC samples from control, chronically alcohol-exposed, and withdrawn rats. To gain insight into the dynamic progression and regulation of withdrawal, we focus on the expression of a subset of functionally relevant genes during the first 48 hours, when behavioral symptoms are most severe. RESULTS In the DVC, expression of this gene subset is essentially normal in chronically alcohol-exposed rats. However, withdrawal results in rapid, large-magnitude expression changes in this group. We observed differential regulation in 86 of the 145 genes measured (59%), some as early as 4 hours into withdrawal. Time series measurements (4, 8, 18, 32, and 48 hours after alcohol removal) revealed dynamic expression responses in immediate early genes, γ-aminobutyric acid type A, ionotropic glutamate, and G-protein coupled receptors and the Ras/Raf signaling pathway. Together, these changes elucidate a complex, temporally coordinated response that involves correlated expression of many functionally related groups. In particular, the expression patterns of Gabra1, Grin2a, Grin3a, and Grik3 were tightly correlated. These receptor subunits share overrepresented transcription factor binding sites for Pax-8 and other transcription factors, suggesting a common regulatory mechanism and a role for these transcription factors in the regulation of neurotransmission within the first 48 hours of alcohol withdrawal. CONCLUSIONS Expression in this gene set is essentially normal in the alcohol-adapted DVC, but withdrawal results in immediate, large-magnitude, and dynamic changes. These data support both increased research focus on the biological ramifications of alcohol withdrawal and enable novel insights into the dynamic withdrawal expression response in this understudied homeostatic control center.
Predictive Properties of Biomarkers GDF-15, NTproBNP, and hs-TnT for Morbidity and Mortality in Patients With Type 2 Diabetes With Nephropathy

OBJECTIVE Although patients with type 2 diabetes (T2D) with nephropathy are at high risk for renal and cardiovascular complications, relevant biomarkers have been poorly identified. Because renal impairment may increase biomarker levels, this potentially confounds associations between biomarker levels and risk. To investigate the predictive value of a biomarker in such a setting, we examined baseline levels of growth differentiation factor-15 (GDF-15), N-terminal prohormone of B-type natriuretic peptide (NTproBNP), and high-sensitivity troponin T (hs-TnT) in relation to renal and cardiovascular risk in T2D patients with nephropathy. RESEARCH DESIGN AND METHODS Eight hundred sixty-one T2D patients from the sulodexide macroalbuminuria (Sun-MACRO) trial were included in our post hoc analysis. Prospective associations of baseline serum GDF-15, NTproBNP, and hs-TnT with renal and cardiovascular events were determined by Cox multiple regression and C-statistic analysis. Renal base models included albumin-to-creatinine ratio (ACR), serum creatinine, hemoglobin, age, and sex. Cardiovascular base models included diastolic blood pressure, ACR, cholesterol, age, and sex. RESULTS The mean (±SD) estimated glomerular filtration rate was 33 ± 9 mL/min/1.73 m2, and the median serum concentration for GDF-15 was 3,228 pg/mL (interquartile range 2,345–4,310 pg/mL), for NTproBNP was 380 ng/L (155–989 ng/L), and for hs-TnT was 30 ng/L (20–47 ng/L). In multiple regression analysis, GDF-15 (hazard ratio [HR] 1.83, P = 0.04), NTproBNP (HR 2.34, P = 0.004), and hs-TnT (HR 2.09, P = 0.014) were associated with renal events, whereas NTproBNP (HR 3.45, P < 0.001) was associated with cardiovascular events. The C-statistic was improved by adding NTproBNP and hs-TNT to the renal model (0.793 vs. 0.741, P = 0.04). For cardiovascular events, the C-statistic was improved by adding NTproBNP alone (0.722 vs. 0.658, P = 0.018). CONCLUSIONS Biomarkers GDF-15, NTproBNP, and hs-TnT associate independently with renal risk, whereas NTproBNP independently predicts cardiovascular risk.
Brain-stem influence on visual response of lagged and nonlagged cells in the cat lateral geniculate nucleus

Abstract This study examined the influence of the pontomesencephalic peribrachial region (PBR) on the visual response properties of cells in the dorsal lateral geniculate nucleus (LGN). The response of single cells to a stationary flashing light spot was recorded with accompanying electrical stimulation of the PBR. The major objectives were to compare the effects of PBR stimulation on lagged and nonlagged cells, to examine how the visual response pattern of lagged cells could be modified by PBR stimulation and to examine whether the physiological criteria used to classify lagged and nonlagged cells are applicable during increased PBR input to the LGN. During PBR stimulation, the visual response was enhanced to a similar degree for lagged and nonlagged cells and the latency to half-rise of the visual response was reduced, particularly for the lagged X cells. The latency to half-fall of the visual response of lagged cells was not changed by PBR stimulation. Accordingly, the division of LGN cells into lagged and nonlagged cells based on visual response latencies was maintained during PBR stimulation. The initial suppression that a visual stimulus evokes in lagged cells was resistant to the effects of PBR stimulation. For the lagged cells, the largest response increase occurred for the initial part of the visual response. For the nonlagged cells, the largest increase occurred for the tonic part of the response. The results support the hypothesis that the differences in temporal response properties between lagged and nonlagged cells belong to the basic distinctions between these cell classes.
Bronchial asthma associated with intestinal parasites.

Abstract Of 201 cases of bronchial asthma, ova or larvae of one or other of three intestinal parasites were found in the stools in 198. Over 90 per cent has ascariasis, 12 patients strongyloidiasis, and two Necator americanus. None of these three parasites were found in a group of allergy-free controls.
Saquinavir drug exposure is not impaired by the boosted double protease inhibitor combination of lopinavir/ritonavir

Objective: To assess the pharmacokinetic interaction of saquinavir and lopinavir/ritonavir. Design: Patients from the Frankfurt HIV cohort with limited reverse transcriptase inhibitor (RTI) options received the protease inhibitor (PI) combination of saquinavir (soft-gel capsules, 1000 mg twice a day) plus lopinavir/ritonavir (400/100 mg twice a day), without RTI (LOPSAQ group). A control group received the same doses of saquinavir and ritonavir plus two to three RTI (RITSAQ group). A steady-state 12 h pharmacokinetic assessment was performed. Methods: Plasma levels of saquinavir, ritonavir and lopinavir were determined by liquid chromatography–tandem mass spectrophotometry. Minimum and maximum plasma concentrations (Cmin and Cmax), the clearance (Cltot) and the area under the concentration time curve (AUC) were calculated. Results: Data were collected from 45 patients (LOPSAQ) and 32 patients (RITSAQ). There was no significant difference between the groups for median saquinavir Cmin, Cmax, Cltot and AUC (LOPSAQ: 543 ng/ml, 2300 ng/ml, 1020 ml/min and 16 977 ng*h/ml; RITSAQ: 427 ng/ml, 2410 ng/ml, 1105 ml/min and 15 130 ng*h/ml). Median ritonavir Cmin, Cmax and AUC were lower, the Cltot was higher in the LOPSAQ group (78 ng/ml, 428 ng/ml and 2972 ng*h/ml, 551 ml/min) compared with RITSAQ (194 ng/ml, 683 ng/ml and 6506 ng*h/ml, 266 ml/min; P < 0.001). Lopinavir levels were similar to historical data. Conclusion: Effective plasma levels of both saquinavir and lopinavir can be achieved by the co-administration of saquinavir soft-gel capsules and lopinavir/ritonavir. This boosted double PI combination could be an effective option for patients with limited RTI options.