Miracle-dz/UniFAR-FTUs huggingface dataset:
Ventilator-associated pneumonia in Iranian intensive care units.

INTRODUCTION Nosocomial pneumonia (NP) and ventilator associated pneumonia (VAP) occur most frequently in intensive care units (ICU). This study seeks to determine the etiological agents of NP and VAP along with their antibacterial susceptibility patterns, and to evaluate the factors contributing to patient mortality. The impact of appropriate therapy in terms of three parameters (body temperature, PaO2/FiO2 ratio and leukocyte count) was also assessed. METHODOLOGY This study involved 836 adult patients admitted to ICUs at the Nemazee Hospital, Shiraz, Iran, over nine months during 2008 and 2009. The inclusion criterion was the commencement of infection at least 48 hours following hospital admission. Clinical parameters including core temperature, leukocyte count. and PaO2/FiO2 ratio were evaluated. Antibiotic sensitivities of the isolated bacteria to a panel of antibiotics were determined using E-test. RESULTS Of 836 cases, only 58 (6.9 %) cases of NP were diagnosed, of which 42 (72 %) were VAP. A. baumannii, MRSA, P. aeruginosa and MSSA were the most prevalent bacteria. Significant correlations between previous antibiotic therapy (p = 0.04), use of corticosteroids (p = 0.02) and attributable mortality were found. A strong correlation between fever abatement and the ratio of PaO2/FiO2 with responses to treatment and outcomes was also evident. CONCLUSIONS Combined treatment with meropenem/imipenem, ciprofloxacin and vancomycin seems to be appropriate and could cover all possible infective agents. To reduce mortality rate, reasonable prescription of antibiotics and corticosteroids could be effective. Furthermore, adopting a strategy to reduce body temperature and PaO2/FiO2 ratio could be beneficial in patients' outcomes.
The Scottish Survey of New Chronic In-patients: Two Year Follow Up

‘New chronic inpatients' (patients aged 18–64 years in hospital more than one but less than six years) were followed-up two years after identification in the catchment areas of 14 psychiatric hospitals, serving 56% of the Scottish population. Nine per cent had died, 71% remained in-patients, and 20% had been discharged; 40% of those discharged had no contact with after-care services, and 37% of those remaining in hospital did not need in-patient care. Discharged patients were younger, had been in hospital a shorter time, and less often had organic brain disease. Only 13% of patients who, when first identified, had been rated at a low functioning level had been discharged; 64% of those remaining in-patients at follow up had such a rating.
Population genetics and spatial structure of the fairy ring fungus Marasmius oreades in a Norwegian sand dune ecosystem

The population genetics and spatial structure of the fairy ring fungus Marasmius oreades (Bolt. : Fr.) Fr. was studied by DNA amplification fingerprinting (DAF). Basidiocarp samples were collected from fairy rings from two separate sand dune systems of about 560 m2 and 1750 m2, respectively, on the Lista Peninsula in southwestern Norway in 1996. Samples were collected after a careful mapping of fairy rings and a vegetation survey of the composition and spatial structure of vascular plants, bryophytes and lichens. DAF with standard arbitrary oligonucleotide primers was used to examine the genetic relationship between basidiocarp samples. The study showed that the fungal population contained a high number of genotypes and that about 90% of the fairy rings represented a separate genet. Both cluster and phylogenetic analyses of DAF amplification products established relationships between fairy rings and showed that genetically similar basidiocarps were found close to each other. Overall results showed a weak correspondence between genotype and spatial distribution and no correspondence between genotype and composition of the surrounding vegetation. Furthermore, the occurrence of the four dominant sand dune grass species was randomly distributed among the localities housing the various fungal genotypes, indicating that the fungus did not exhibit genotypic specialization to the various grass species that could host it as a pathogen. Results show that establishment of new individuals generally was mediated by basidiospore dispersal and not by fragmenting dikaryotic, vegetative mycelium, as previously proposed.
Substance P in Polymicrobial Sepsis: Molecular Fingerprint of Lung Injury in Preprotachykinin-A−/− Mice

Deletion of mouse preprotachykinin-A (PPTA), which encodes mainly for neuropeptide substance P, has been shown to protect against lung injury and mortality in sepsis. This study explored microarray-based differential gene expression profiles in mouse lung tissue 8 h after inducing microbial sepsis and the effect of PPTA gene deletion. A range of genes differentially expressed (more than two-fold) in microarray analysis was assessed, comparing wild-type and PPTA-knockout septic mice with their respective sham controls, and the data were further validated. Genetic deletion of substance P resulted in a significantly different expression profile of genes involved in inflammation and immunomodulation after the induction of sepsis, compared with wild-type mice. Interestingly, apart from the various proinflammatory mediators, the antiinflammatory cytokine interleukin-1 receptor antagonist gene (IL1RN) was also elevated much more in PPTA−/− septic mice. In addition, semiquantitative RT-PCR analysis supported the microarray data. The microarray data imply that the elevated levels of inflammatory gene expression in the early stages of sepsis in PPTA-knockout mice are possibly aimed to resolve the infection without excessive immunosuppression. As scientists are divided over the effects of pro- and antiinflammatory mediators in sepsis, it seems prudent to define the status depending on a complete genome profile. This is the first report exploring pulmonary gene expression profiles using microarray analysis in PPTA-knockout mice subjected to cecal ligation and puncture-induced sepsis and providing additional biological insight into the protection received against lung injury and mortality.
How hippocampus and cortex contribute to recognition memory: Revisiting the complementary learning systems model

We describe how the Complementary Learning Systems neural network model of recognition memory (Norman and O'Reilly (2003) Psychol Rev 104:611–646) can shed light on current debates regarding hippocampal and cortical contributions to recognition memory. We review simulation results illustrating three critical differences in how (according to the model) hippocampus and cortex contribute to recognition memory, all of which derive from the hippocampus' use of pattern separated representations. Pattern separation makes the hippocampus especially well‐suited for discriminating between studied items and related lures; it makes the hippocampus especially poorly suited for computing global match; and it imbues the hippocampal ROC curve with a Y‐intercept > 0. We also describe a key boundary condition on these differences: When the average level of similarity between items in an experiment is very high, hippocampal pattern separation can fail, at which point the hippocampal model will start to behave like the cortical model. We describe the implications of these simulation results for extant debates over how to describe hippocampal versus cortical contributions and how to measure these contributions. © 2010 Wiley‐Liss, Inc.
Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency

Significance Cockayne syndrome (CS) and xeroderma pigmentosum (XP) are photosensitive diseases with mutations in the nucleotide excision repair (NER) pathway. XP patients have a very high incidence of UV-induced skin cancer, but CS patients have never been reported to develop cancer. Cultured cells from both diseases have similar sensitivity to UV-induced cytotoxicity. We examined UV-induced mutagenesis in cells from XP patients with mutations in the global genome repair branch of the NER pathway (XP-C cells) and CS primary cells using duplex sequencing for high sensitivity without selection. XP-C cells showed increased UV-induced mutation frequencies compared with normal cells, consistent with their increased cancer incidence. CS cells, in contrast, showed no elevated mutagenesis. Therefore the absence of cancer in CS patients results from the absence of increased mutations following UV exposure. Cockayne syndrome (CS) and xeroderma pigmentosum (XP) are human photosensitive diseases with mutations in the nucleotide excision repair (NER) pathway, which repairs DNA damage from UV exposure. CS is mutated in the transcription-coupled repair (TCR) branch of the NER pathway and exhibits developmental and neurological pathologies. The XP-C group of XP patients have mutations in the global genome repair (GGR) branch of the NER pathway and have a very high incidence of UV-induced skin cancer. Cultured cells from both diseases have similar sensitivity to UV-induced cytotoxicity, but CS patients have never been reported to develop cancer, although they often exhibit photosensitivity. Because cancers are associated with increased mutations, especially when initiated by DNA damage, we examined UV-induced mutagenesis in both XP-C and CS cells, using duplex sequencing for high-sensitivity mutation detection. Duplex sequencing detects rare mutagenic events, independent of selection and in multiple loci, enabling examination of all mutations rather than just those that confer major changes to a specific protein. We found telomerase-positive normal and CS-B cells had increased background mutation frequencies that decreased upon irradiation, purging the population of subclonal variants. Primary XP-C cells had increased UV-induced mutation frequencies compared with normal cells, consistent with their GGR deficiency. CS cells, in contrast, had normal levels of mutagenesis despite their TCR deficiency. The lack of elevated UV-induced mutagenesis in CS cells reveals that their TCR deficiency, although increasing cytotoxicity, is not mutagenic. Therefore the absence of cancer in CS patients results from the absence of UV-induced mutagenesis rather than from enhanced lethality.
Implementation of Input-Process-Output Model for Measuring Information System Project Success

Measurement of the information system (IS) project success has become the interesting topic for researchers and practitioners since the Standish Group published their findings in 1994. Project success theory is the main concept in this topic, but this theory is still an ambiguous concept and lack in agreement among researchers and practitioners. They are also still tend to focus on single or partial dimension. Therefore, they did not get a clear picture of the system measurements. This study developed an alternative model of the project success measurement based on input-process-output (IPO) model. The development was conducted using comparison, adoption, adaptation, and combination the previous theories and models: Davis's IPO model, the project success theories, Delone and McLean' model, and the project classificatory framework. As indicated in most studies that most of models are developed using the previous theories and models rather than on empirical proofs. The result is a IS project success model consisting of 9 variables and 36 relationships among the variables. Although, the model is only a conceptual model, but it was developed completely and coherently considering three main aspects of project success measurement, namely: processional and causal models, project success theories, and the influence concept of project environment.
Overexpression of the &mgr;-Opioid Receptor in Human Non-Small Cell Lung Cancer Promotes Akt and mTOR Activation, Tumor Growth, and Metastasis

Background: Recent epidemiologic studies suggesting that there were differences in cancer recurrence contingent on anesthetic regimens have raised the possibility that &mgr;-opioid agonists can influence cancer progression. Based on our previous studies indicating the &mgr;-opioid receptor (MOR) is up-regulated in several types of non-small cell lung cancer, this study examined the functional significance of MOR overexpression to elucidate a possible mechanism for the epidemiologic findings. Methods: Stable vector control and MOR1 overexpressing human bronchioloalveolar carcinoma cells were evaluated using immunoblot analysis, proliferation and transendothelial extravasation assays with or without Akt inhibitor, mTOR inhibitor (temsirolimus), or the peripheral MOR antagonist, methylnaltrexone. In human lung cancer xenograft models, primary tumor growth rates and lung metastasis were analyzed using consecutive tumor volume measurements and nestin immunoreactivity in lungs of the nude mouse model. Results: The authors provide evidence that MOR is an important regulator of lung cancer progression. MOR overexpression increased Akt and mTOR activation, proliferation, and extravasation in human bronchioloalveolar carcinoma cells. In vivo, overexpression of MOR in human bronchoalveolar carcinoma cells increased primary tumor growth rates in nude mice by approximately 2.5-fold and lung metastasis by approximately 20-fold compared with vector control cells (n = 4 per condition). Conclusions: The overexpression data suggest a possible direct effect of MOR on Akt and mTOR activation and lung cancer progression. Such an effect provides a plausible explanation for the epidemiologic findings. The authors' observations further suggest that exploration of MOR in non-small cell lung carcinoma merits further study both as a diagnostic and therapeutic option.
Calcium influx in contracting and paralyzed frog twitch muscle fibers

Calcium uptake produced by a potassium contracture in isolated frog twitch fibers was 6.7 +/- 0.8 pmol in 0.7 cm of fiber (mean +/- SEM, 21 observations) in the presence of 30 microM D600. When potassium was applied to fibers paralyzed by the combination of 30 microM D600, cold, and a prior contracture, the calcium uptake fell to 3.0 +/- 0.7 pmol (11): the fibers were soaked in 45Ca in sodium Ringer for 3 min before 45Ca, in a potassium solution, was added for 2 min; each estimate of uptake was corrected for 5 min of resting influx, measured from the same fiber (average = 2.3 +/- 0.3 pmol). The calcium influx into paralyzed fibers is unrelated to contraction. This voltage-sensitive, slowly inactivating influx, which can be blocked by 4 mM nickel, has properties similar to the calcium current described by several laboratories. The paired difference in calcium uptake between contracting and paralyzed fibers, 2.9 +/- 0.8 pmol (16), is a component of influx related to contraction. Its size varies with contracture size and it occurs after tension production: 45Ca applied immediately after contracture is taken up in essentially the same amounts as 45Ca added before contraction. This delayed uptake is probably a "reflux" refilling a binding site on the cytoplasmic side of the T membrane, which had been emptied during the prior contracture, perhaps to initiate it. We detect no component of calcium uptake related to excitation-contraction coupling occurring before or during a contracture.
Prognosis of the Midlife-Elderly from ECG Testing to Gastroesophageal Reflux Disease and Coronary Artery Disease

C l i n M e d International Library Citation: Mohammed SB, Gadad A, Nayak BS, Beharry V (2016) Prognosis of the MidlifeElderly from ECG Testing to Gastroesophageal Reflux Disease and Coronary Artery Disease. J Fam Med Dis Prev 2:029 Received: December 24, 2015: Accepted: March 29, 2016: Published: April 01, 2016 Copyright: © 2016 Mohammed SB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Mohammed et al. J Fam Med Dis Prev 2016, 2:029
Series Divisions of Research & Statistics and Monetary Affairs Federal Reserve Board , Washington , D . C . Mergers and Sequential Innovation : Evidence from Patent Citations

An extensive literature has investigated the effect of market structure on innovation. A persistent concern is that market structure may be endogenous to innovation. Firms may choose to merge so as to capture information spillovers or they may choose to merge so as to dampen competition in innovation. These two scenarios have very different welfare implications. This paper attempts to distinguish between the two scenarios empirically, looking at recent mergers among public companies in the United States. Using patent citation data, I find evidence that firms increase their rate of sequential innovation in the years preceding a merger, and reduce their rate of sequential innovation in the years following a merger. This suggests that mergers are motivated more by the desire to dampen competition than by the desire to capture information spillovers. I use citation-based measures of patent value to shed light on the welfare implications. The question is relevant for policy, as the FTC and DOJ frequently cite innovation as a reason for concern about a merger. JEL codes: L1, L4, O3. ∗Email: jessica.c. stahl@frb.gov. This is a revised version of a chapter of my Ph.D. dissertation at Boston University. I would like to thank my advisor, Marc Rysman. I also received helpful comments from Iain Cockburn, Megan MacGarvie, Jordi Jaumandreu, and seminar participants at Boston University and NBER. All errors are my own. The analysis and conclusions set forth are those of the author and do not indicate concurrence by the Federal Reserve System.
Easy quantitative assessment of genome editing by sequence trace decomposition

The efficacy and the mutation spectrum of genome editing methods can vary substantially depending on the targeted sequence. A simple, quick assay to accurately characterize and quantify the induced mutations is therefore needed. Here we present TIDE, a method for this purpose that requires only a pair of PCR reactions and two standard capillary sequencing runs. The sequence traces are then analyzed by a specially developed decomposition algorithm that identifies the major induced mutations in the projected editing site and accurately determines their frequency in a cell population. This method is cost-effective and quick, and it provides much more detailed information than current enzyme-based assays. An interactive web tool for automated decomposition of the sequence traces is available. TIDE greatly facilitates the testing and rational design of genome editing strategies.
Effect of rosiglitazone on cardiac electrophysiology, infarct size and mitochondrial function in ischaemia and reperfusion of swine and rat heart

Rosiglitazone, a peroxisome proliferator‐activated receptor γ agonist, has been used to treat type 2 diabetes. Despite debates regarding its cardioprotection, the effects of rosiglitazone on cardiac electrophysiology are still unclear. This study determined the effect of rosiglitazone on ventricular fibrillation (VF) incidence, VF threshold (VFT), defibrillation threshold (DFT) and mitochondrial function during ischaemia and reperfusion. Twenty‐six pigs were used. In each pig, either rosiglitazone (1 mg kg−1) or normal saline solution was administered intravenously for 60 min. Then, the left anterior descending coronary artery was ligated for 60 min and released to promote reperfusion for 120 min. The cardiac electrophysiological parameters were determined at the beginning of the study and during the ischaemia and reperfusion periods. The heart was removed, and the area at risk and infarct size in each heart were determined. Cardiac mitochondria were isolated for determination of mitochondrial function. Rosiglitazone did not improve the DFT and VFT during the ischaemia–reperfusion period. In the rosiglitazone group, the VF incidence was increased (58 versus 10%) and the time to the first occurrence of VF was decreased (3 ± 2 versus 19 ± 1 min) in comparison to the vehicle group (P < 0.05). However, the infarct size related to the area at risk in the rosiglitazone group was significantly decreased (P < 0.05). In the cardiac mitochondria, rosiglitazone did not alter the level of production of reactive oxygen species and could not prevent mitochondrial membrane potential changes. Rosiglitazone increased the propensity for VF, and could neither increase defibrillation efficacy nor improve cardiac mitochondrial function.
Expression patterns of synaptic vesicle protein 2A in focal cortical dysplasia and TSC‐cortical tubers

Purpose: Synaptic vesicle protein 2A (SV2A), the binding site for the antiepileptic drug (AED) levetiracetam, has been shown to be involved in the control of neuronal excitability. The aim of the study was to define the expression and cell‐specific distribution of SV2A in developmental focal lesions associated with medically intractable epilepsy.
Charity and the American Jury: Exploring the Relationship Between Plaintiffs Need-Based Arguments and Juror Verdicts in Medical Malpractice Suits

Critics of the American jury system argue that jurors have “turned the legal system into a charity program” where jurors' verdicts are based more on plaintiff “neediness” than on the factual merits of the case. This study tests this and associated claims by varying the plaintiff attorney's need-based arguments in a simulated medical malpractice case. While findings indicated that the mock jurors were aware of the plaintiffs need, the results did not support claims that jurors are swayed by such arguments. Other findings of interest include the following: women allocated greater fault to the physician than did men; the amount of fault awarded to the physician was associated with participants' view of the physician's ability to pay; and, participants exposed to the high-need condition viewed the plaintiff as less responsible for her health care than those exposed to other conditions.
An Increased Burden of Common and Rare Lipid-Associated Risk Alleles Contributes to the Phenotypic Spectrum of Hypertriglyceridemia

Objective—Earlier studies have suggested that a common genetic architecture underlies the clinically heterogeneous polygenic Fredrickson hyperlipoproteinemia (HLP) phenotypes defined by hypertriglyceridemia (HTG). Here, we comprehensively analyzed 504 HLP-HTG patients and 1213 normotriglyceridemic controls and confirmed that a spectrum of common and rare lipid-associated variants underlies this heterogeneity. Methods and Results—First, we demonstrated that genetic determinants of plasma lipids and lipoproteins, including common variants associated with plasma triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) from the Global Lipids Genetics Consortium were associated with multiple HLP-HTG phenotypes. Second, we demonstrated that weighted risk scores composed of common TG-associated variants were distinctly increased across all HLP-HTG phenotypes compared with controls; weighted HDL-C and LDL-C risk scores were also increased, although to a less pronounced degree with some HLP-HTG phenotypes. Interestingly, decomposition of HDL-C and LDL-C risk scores revealed that pleiotropic variants (those jointly associated with TG) accounted for the greatest difference in HDL-C and LDL-C risk scores. The APOE E2/E2 genotype was significantly overrepresented in HLP type 3 versus other phenotypes. Finally, rare variants in 4 genes accumulated equally across HLP-HTG phenotypes. Conclusion—HTG susceptibility and phenotypic heterogeneity are both influenced by accumulation of common and rare TG-associated variants.