Miracle-dz/UniFAR-FTUs huggingface dataset:
No apparent association between bipolar disorder and cancer in a large epidemiological study of outpatients in a managed care population

An association between bipolar disorder (BD) and cancer risk has been reported. The purpose of this study was to investigate this association through linkage analysis of a national HMO database and a national cancer registry. All members of the Leumit Health Services (LHS) HMO of Israel from 2000 to 2012 were included. Members with a recorded diagnosis of BD and a record of at least one written or dispensed prescription for pharmacotherapy for treatment of BD were classified as patients with BD. We linked the LHS population with the Israel National Cancer Registry database to capture all cases of cancer reported. Standardized incidence ratios (SIRs) for cancer in the BD population as compared with non-BD LHS members were calculated. A total of 870 323 LHS members were included in the analysis; 3304 of whom met the criteria for inclusion in the BD arm. We identified 24 515 and 110 cancer cases among members without BD and with BD, respectively. Persons with BD were no more likely than other HMO members to be diagnosed with cancer during the follow-up period [SIR, males=0.91, 95% confidence interval (CI): 0.66–1.22; SIR, females=1.15, 95% CI: 0.89–1.47]. Sensitivity analysis using different criteria for positive BD classification (lithium treatment alone or registered physician diagnosis) had no effect on the estimate of cancer risk. A nonstatistically significant association between breast cancer and BD among women was observed (SIR=1.24, 95% CI: 0.79–1.86). These findings do not corroborate previously reported associations between BD and elevated cancer risk.
Is It the Best of Times or the Worst

The continuing implosion of the U.S. housing market has caused many forecasters to trim their economic-growth estimates for this year and next. Although none is openly using the R-word, most expect a period of substandard growth extending at least through the first half of 2008. The great uncertainty in the economic outlook is the extent to which housing-related woes and the associated financial-market turmoil might impact other sectors, notably business investment and consumer spending.
Using external and internal locking plates in a two-stage protocol for treatment of segmental tibial fractures.

BACKGROUND The tibial segmental fractures usually follow high-energy trauma and are often associated with many complications. We designed a two-stage protocol for these complex injuries. The aim of this study was to assess the outcome of tibial segmental fractures treated according to this protocol. METHODS A prospective series of 25 consecutive segmental tibial fractures were treated using a two-stage procedure. In the first stage, a low-profile locking plate was applied as an external fixator to temporarily immobilize the fractures after anatomic reduction had been achieved followed by soft-tissue reconstruction. The second stage involved definitive internal fixation with a locking plate using a minimally invasive percutaneous plate osteosynthesis technique. The median follow-up was 32 months (range, 20-44 months). RESULTS All fractures achieved union. The median time for the proximal fracture union was 23 weeks (range, 12-30 weeks) and that for distal fracture union was 27 weeks (range, 12-46 weeks; p = 0.08). Functional results were excellent in 21 patients and good in 4 patients. There were three cases of delayed union of distal fracture. Valgus malunion >5 degrees occurred in two patients, and length discrepancy >1 cm was observed in two patients. Pin tract infection occurred in three patients. CONCLUSIONS Use of the two-stage procedure for treatment of segmental tibial fractures is recommended. Surgeons can achieve good reduction with stable temporary fixation, soft-tissue reconstruction, ease of subsequent definitive fixation, and high union rates. Our patients obtained excellent knee and ankle joint motion, good functional outcomes, and a comfortable clinical course.
Prospective Cohort Study on the Effectiveness of Influenza and Pneumococcal Vaccines in Preventing Pneumonia Development and Hospitalization

ABSTRACT Pneumonia and acute exacerbation of chronic illness are leading causes of influenza-related hospitalization. Therefore, influenza and pneumococcal vaccinations are strongly recommended for adults with comorbidities. Using a hospital-based influenza surveillance system, we performed a multicenter, prospective cohort study of patients visiting emergency rooms with influenza-like illness (ILI) during the influenza epidemic period in 2013 to 2014. Patients aged ≥19 years were enrolled, and clinical data were collected. Multivariate analyses were performed to estimate the effectiveness of influenza and pneumococcal vaccination in preventing pneumonia development and hospitalization. During study periods, 2,262 patients with ILI were registered. Among 2,217 patients with available vaccination records, 31.9% (707 patients) and 9.7% (216 patients) had received influenza and pneumococcal vaccines, respectively. Among patients who had been administered a pneumococcal vaccine, 94.4% had received the 23-valent polysaccharide vaccine (PPV23). The adjusted rates of effectiveness of the influenza vaccine for preventing pneumonia development and hospitalization were 64.0% (95% confidence interval [CI] = 29% to 81%) and 35.0% (95% CI = 12% to 52%), respectively. Pneumococcal vaccination did not reduce pneumonia development or hospitalization. In conclusion, influenza rather than PPV23 vaccination may reduce pneumonia development and hospitalization in patients with preceding ILI.
Serum Ethanol Levels in Patients with Moderate to Severe Traumatic Brain Injury Influence Outcomes: A Surprising Finding

Animal studies routinely demonstrate an alcohol (ETOH) -mediated increase in survival after experimental traumatic brain injury (TBI). Recent clinical studies also suggest ETOH plays a neuroprotective role in moderate to severe TBI. We sought to investigate the relationship between ETOH and outcomes in patients with moderate to severe TBI using a countywide database. The Los Angeles County Trauma System database was queried for all adult (older than 14 years) patients with isolated moderate to severe TBI trauma (head Abbreviated Injury Score [AIS] 3 or greater, all other AIS 3 or less) who had ETOH levels measured on admission between 1998 and 2005. A total of 7304 patients were evaluated with 3219 (44.1%) patients testing positive for serum ETOH. ETOH-positive patients with TBI had a significantly lower mortality rate compared with ETOH negative patients (8.5 vs 10.5%, P = 0.005). Even after logistic regression analysis, a positive ETOH was associated with reduced mortality (adjusted OR 0.82, 95% CI: 0.69-0.99, P = 0.035). Therefore, a positive serum ETOH level was independently associated with significantly improved survival in patients with isolated moderate to severe TBI. The neuroprotective role ETOH plays in TBI is in contrast to previous findings and deserves further attention as a potential therapeutic.
Pharmacology of the endothelium in ischemia-reperfusion and circulatory shock.

Endothelial dysfunction is an important early-recurring phenomenon in virtually all forms of ischemia-reperfusion, including a variety of circulatory shock states. The dysfunction appears to be triggered within 2.5 min of the endothelial generation of a large burst of superoxide radicals. However, the initial dysfunction may be amplified by neutrophil-generated factors including oxygen-derived free radicals, cytokines, proteases, and lipid mediators. Moreover, adhesive molecules on the surface of the PMN, along with their ligands on the endothelial cell membrane, appear to promote endothelial dysfunction in ways that may go beyond the adherence of neutrophils on the endothelial surface. These interactions remain to be elucidated but may involve intricate cell signaling pathways. A variety of pharmacologic agents exert endothelial protective effects in ischemia-reperfusion and circulatory shock states. Table 1 summarizes these agents and indicates the major mechanism of preservation of the endothelium. These substances can be classified into three broad categories: (a) substances replacing endogenous cytoprotective agents of endothelial origin including prostacyclin (PGI2), endothelium-derived relaxing factor (EDRF), and adenosine: the endothelium protecting agents include these substances as well as stable analogs of PGI2, and nitric oxide donors; (b) substances that inhibit pro-inflammatory mediators of endothelial origin: the pro-inflammatory agents are primarily platelet activating factor (PAF) and oxygen-derived free radicals (e.g. superoxide radicals) although other mediators may be involved. The therapeutic agents useful in this area are PAF receptor antagonists and free radical scavengers (e.g. superoxide dismutase); (c) substances that inhibit neutrophils or neutrophil-derived mediators: the major neutrophil-derived mediators are oxygen-derived free radicals, cytokines (e.g. TNF alpha and IL-1 beta), proteases (e.g. elastase), and lipid mediators (e.g. LTB4). In addition, adhesive molecules on the neutrophil surface and their endothelial ligands promote endothelial dysfunction and the action of adherent neutrophils. Agents that inhibit some of these mediators are transforming growth factor-beta (TGF-beta), elastase inhibitors, leukotriene B4 (LTB4) receptor antagonists and monoclonal antibodies to adhesive proteins (e.g. anti-CD18, anti-ICAM-1). Further work is needed to clarify these findings and to determine the physiologic and pathophysiologic interactions among these diverse agents. This topic of endothelial dysfunction represents a fertile area for further investigation to elucidate the complex mechanisms of neutrophil-endothelial interactions. These interactions lead to neutrophil adherence to the endothelium, neutrophil migration into the underlying tissues, and subsequent tissue injury (e.g. myocardial reperfusion injury). (ABSTRACT TRUNCATED AT 400 WORDS)
Dasatinib, a Multikinase Inhibitor: Therapy, Safety, and Appropriate Management of Adverse Events

Tyrosine kinase inhibitors are the standard of care for the treatment of chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia. Dasatinib is a second-generation tyrosine kinase inhibitor that has been shown to be efficacious in treatment of patients with chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia who are resistant or intolerant to frontline imatinib. In clinical trials of dasatinib, the adverse events that arise during therapy are mostly mild to moderate in severity and are usually reversible and manageable with appropriate intervention. Cytopenias can be treated with dose modification or interruption. Pleural effusions can be effectively managed with prompt delivery of supportive care and dose modification. Patients at risk of cardiac abnormalities or bleeding-related events require careful monitoring. Pharmacokinetic analysis of dasatinib indicates interactions with a number of other agents and a complete treatment history should be taken before initiating therapy because mitigating drug-drug interactions are critical for patient safety.
Microarray analysis sheds light on the dedifferentiating role of agouti signal protein in murine melanocytes via the Mc1r

The melanocortin-1 receptor (MC1R) is a key regulator of pigmentation in mammals and is tightly linked to an increased risk of skin cancers, including melanoma, in humans. Physiologically activated by α-melanocyte stimulating hormone (αMSH), MC1R function can be antagonized by a secreted factor, agouti signal protein (ASP), which is responsible for the lighter phenotypes in mammals (including humans), and is also associated with increased risk of skin cancer. It is therefore of great interest to characterize the molecular effects elicited by those MC1R ligands. In this study, we determined the gene expression profiles of murine melan-a melanocytes treated with ASP or αMSH over a 4-day time course using genome-wide oligonucleotide microarrays. As expected, there were significant reductions in expression of numerous melanogenic proteins elicited by ASP, which correlates with its inhibition of pigmentation. ASP also unexpectedly modulated the expression of genes involved in various other cellular pathways, including glutathione synthesis and redox metabolism. Many genes up-regulated by ASP are involved in morphogenesis (especially in nervous system development), cell adhesion, and extracellular matrix-receptor interactions. Concomitantly, ASP enhanced the migratory potential and the invasiveness of melanocytic cells in vitro. These results demonstrate the role of ASP in the dedifferentiation of melanocytes, identify pigment-related genes targeted by ASP and by αMSH, and provide insights into the pleiotropic molecular effects of MC1R signaling that may function during development and may affect skin cancer risk.
A Novel ECMS and Combined Cost Map Approach for High-Efficiency Series Hybrid Electric Vehicles

The main aim in the control of a hybrid electric vehicle (HEV) is to decrease the fuel consumption and emissions without significant loss of driving performance. The performance of the vehicle in terms of fuel economy and emissions is very much dependent on the vehicle's supervisory control strategy. In this paper, the equivalent consumption minimization strategy (ECMS) is developed with a novel approach for the charge sustaining of the batteries to provide an overall improved optimization performance for series hybrid electric vehicles (SHEVs), considering the efficiencies of the internal combustion engine (ICE), generator, and battery. Another novelty is the development of a combined map, which simultaneously facilitates the optimization of the fuel consumption and multiple emission components, unlike most past studies that have concentrated on one component at a time. After the derivation of the cost map, the algorithm is divided into two main parts. The first part optimizes the engine-generator set (GENSET), and the second part determines how much power is needed from the GENSET according to the ECMS. The algorithm is implemented using generic emission and fuel consumption maps of an actual mid-sized series hybrid bus to reduce the desired emissions. The hybrid electric vehicle in consideration is converted from a conventional bus that is driven by an ICE. The performance of the novel ECMS strategy is compared with the conventional vehicle, as well as the SHEV version that is driven by an on-off strategy. In addition to reduced fuel consumption, the results of this paper demonstrate a significant reduction of 14.58% in CO2 production with ECMS, whereas the on-off control strategy achieves only 6.47% reduction over the conventional vehicle.
International migration and innovation diffusion: an eclectic survey

ABSTRACT International migration and innovation diffusion: an eclectic survey. Regional Studies. In the new era of international mass migration, the role of highly skilled individuals in diffusing innovation has attracted considerable attention. Using economic history studies as a template, the paper organizes several strands of the literature around three main themes: the distinction between mobility and migration; the directions of flows; and their contents. Migration supports diffusion from origin to host countries, but also in the opposite direction, as well as within and across destinations. A research agenda is proposed with special focus on the importance of social ties among migrants and the distinction between access to general information and knowledge exchanges.
Herbivores and Plant Diversity

We study spatial lottery models of competition between two plant species in which competitive ability is affected by levels of herbivory. Herbivory may enhance plant diversity in two qualitatively different ways. The first is global frequency dependence; the level of herbivory suffered by a plant decreases as the species becomes rare. Second, spatial variability in levels of herbivory can create ephemeral, local refuges for herbivory for each plant species. Both of these mechanisms operate only if there is not a negative correlation between a plant's palatability and its competitive ability. Both mechanisms also require that herbivores have sufficiently strong diet preferences (or, equivalently, that the plants have sufficiently different grazing tolerances). If there is no relationship between palatability and competitive ability, then plant diversity is a monotonically increasing function of the herbivore's degree of monophagy. In contrast, if there is a positive correlation between palatability and competitive ability, then the diversity/degree-of-monophagy relationship may be either monotonically increasing or humped.
Effects of dietary methionine on performance, egg quality and glutathione redox system in egg-laying ducks

Abstract In this study, 6 dietary DL-methionine (Met) levels (2.5, 3.0, 3.5, 4.0, 4.5 and 5.0 g/kg) were tested to estimate the dietary Met requirements of Longyan ducks from 19 to 46 weeks of age, and to investigate its effect on the glutathione redox system. In total, 1080 Longyan ducks aged 19 weeks were allocated randomly to the 6 dietary treatments, where each treatment comprised 6 replicate pens with 30 ducks per pen. Met had no effects on egg production, yolk weight, yolk colour or the glutathione redox system, but the egg weight, egg mass and feed conversion ratio (FCR) were improved significantly by dietary Met supplementation. As the dietary Met concentration increased, the eggshell thickness and breaking strength decreased significantly, whereas the albumen weight increased significantly. According to broken-line regression analysis, the optimum Met requirements for egg weight, egg mass, FCR and albumen weight are 686, 661, 658 and 731 mg/bird/d, respectively, with a dietary crude protein level of 170 g/kg.
Identification and nitrogen regulation of the cyanase gene from the cyanobacteria Synechocystis sp. strain PCC 6803 and Synechococcus sp. strain PCC 7942

An open reading frame (slr0899) on the genome of Synechocystis sp. strain PCC 6803 encodes a polypeptide of 149 amino acid residues, the sequence of which is 40% identical to that of cyanase from Escherichia coli. Introduction into a cyanase-deficient E. coli strain of a plasmid-borne slr0899 resulted in expression of low but significant activity of cyanase. Targeted interruption of a homolog of slr0899 from Synechococcus sp. strain PCC 7942, encoding a protein 77% identical to that encoded by slr0899, resulted in loss of cellular cyanase activity. These results indicated that slr0899 and its homolog in the strain PCC 7942 represent the cyanobacterial cyanase gene (designated cynS). While cynS of strain PCC 6803 is tightly clustered with the four putative molybdenum cofactor biosynthesis genes located downstream, cynS of strain PCC 7942 was found to be tightly clustered with the two genes located upstream, which encode proteins similar to the subunits of the cyanobacterial nitrate-nitrite transporter. In both strains, cynS was transcribed as a part of a large transcription unit and the transcription was negatively regulated by ammonium. Cyanase activity was low in ammonium-grown cells and was induced 7- to 13-fold by inhibition of ammonium fixation or by transfer of the cells to ammonium-free media. These findings indicated that cyanase is an ammonium-repressible enzyme in cyanobacteria, the expression of which is regulated at the level of transcription. Similar to other ammonium-repressible genes in cyanobacteria, expression of cynS required NtcA, a global nitrogen regulator of cyanobacteria.
Intraischemic hypothermia decreases the release of glutamate in the cores of permanent focal cerebral infarcts.

The cerebroprotective effects of hypothermia in focal models of ischemia are well established, but little is known about the underlying mechanisms of this form of brain protection. Cortical cooling in global transient ischemic models suggests that hypothermia limits glutamate excitotoxicity by decreasing the release of glutamate during ischemia. Few studies have examined glutamate release in the more physiological model of permanent focal ischemia. In this study, we used a rat model of middle cerebral artery occlusion (MCAO) of permanent focal ischemia. Extracellular glutamate concentration was analyzed bilaterally by microdialysis for 30 minutes before MCAO to 120 minutes after MCAO. Normothermic animals (n = 13) had a baseline glutamate concentration of 9.23 +/- 2.5 mumol/ml (mean +/- standard error of the mean) before MCAO. Extracellular glutamate rose quickly after vessel occlusion and peaked at 33.95 +/- 6.3 mumol/ml 30 minutes after MCAO. By 60 minutes after MCAO, this level had decreased to 25.14 +/- 6.3 mumol/ml; glutamate levels decreased slightly to 21.35 +/- 6.8 mumol/ml by 120 minutes. Hypothermic animals (n = 11) had an initial extracellular glutamate concentration of 5.22 +/- 1.3 mumol/ml before MCAO. This value rose gradually to a maximum of 10.69 +/- 3.3 microns/ml at 50 minutes after MCAO and then returned to a baseline value of 2.58 +/- 1.2 mumol/ml by 120 minutes. Contralateral control glutamate dialysates in the normothermic and hypothermic groups remained near baseline throughout the experimental period. The mean percentages of right hemispheric volumes occupied by infarcts were 11.96 +/- 1.68% in the hypothermic group and 19.77 +/- 2.03% in the normothermic animals. (ABSTRACT TRUNCATED AT 250 WORDS)
Variation and heritability of Hb F and F‐cells among β‐thalassemia heterozygotes in Hong Kong

Enhanced fetal hemoglobin (Hb F) production can partially compensate for the lack of adult hemoglobin (Hb A) in patients with β‐thalassemia major or intermedia, and ameliorate the clinical severity of these diseases. To further elucidate factors governing Hb F levels, we evaluated demographic, clinical, laboratory, and genetic characteristics in 241 unrelated adult β‐thalassemia carriers in Hong Kong. They had wide variations in Hb F and F‐cell numbers skewing toward higher levels. Individuals who coinherited the Xmn IT‐allele in the Gγ‐globin gene promoter had higher Hb F and more F‐cells compared with those lacking the Xmn I T‐allele. However, both groups exhibited a similarly wide spread of Hb F and F‐cells. The correlation of Hb F and F‐cells corresponded well to both linear and exponential models, suggesting multiple mechanisms for Hb F augmentation. The heritabilities of Hb F and F‐cells were calculated in 66 families (111 parents who were β‐thalassemia carriers and 82 asymptomatic offspring) to be 0.7 to 0.9. The Xmn I polymorphism accounted for 9% of the Hb F and 13% of the F‐cell heritabilities. These results suggest that these family members are well suited for genome wide association studies that will identify genetic loci regulating Hb F production, and likely novel pharmacological targets for reactivating Hb F production in adults. Am. J. Hematol. , 2008. © 2008 Wiley‐Liss, Inc.