Miracle-dz/UniFAR-FTUs huggingface dataset:
Social Networks of Alaska Fishing Communities

Abstract Fishing community social networks function as channels for transfer of fishery knowledge, resources, and business transactions that help mitigate risks and shocks associated with altered access to fishery resources. Research on such networks in Alaska is limited despite their cultural importance and community reliance on fisheries. We contribute to scholarship of fishery social networks by assessing Alaska fishing community perspectives of challenges related to fisheries policy and management, and the existing social networks that aid in overcoming these challenges. Our findings show that the greatest challenges fishing communities face pertaining to fishery management are high costs of participating in catch share programs, restricted subsistence fishing activity due to decline in salmon, and complex regulations. Social networks exist for coping with these challenges; fishery information, and resources such as food, fuel and medicines are shared between communities. However, networks for accessing fishery support services are centralized in fewer larger communities and hubs such as Anchorage. Smaller and remote communities are the most compromised in this regard given the distance they must travel to access fishery support services. Leveraging social networks for sharing resources and improving fishery support services in smaller communities will increase their adaptive capacity and ability to maintain participation in Alaska fisheries.
Balancing inflammatory, lipid, and xenobiotic signaling pathways by VSL#3, a biotherapeutic agent, in the treatment of inflammatory bowel disease

Background: The interleukin 10 knockout mouse (IL10‐KO) is a model of human inflammatory bowel disease (IBD) used to study host microbial interactions and the action of potential therapeutics. Using Affymetrix data analysis, important signaling pathways and transcription factors relevant to gut inflammation and antiinflammatory probiotics were identified. Methods: Affymetrix microarray analysis on both wildtype (WT) and IL10‐KO mice orally administered with and without the probiotic VSL#3 was performed and the results validated by real‐time polymerase chain reaction (PCR), immunocytochemistry, proteomics, and histopathology. Changes in metabolically active bacteria were assessed with denaturing gradient gel electrophoresis (DGGE). Results: Inflammation in IL10‐KO mice was characterized by differential regulation of inflammatory, nuclear receptor, lipid, and xenobiotic signaling pathways. Probiotic intervention resulted in downregulation of CXCL9 (fold change [FC] = −3.98, false discovery rate [FDR] = 0.019), CXCL10 (FC = −4.83, FDR = 0.0008), CCL5 (FC = −3.47, FDR = 0.017), T‐cell activation (Itgal [FC = −4.72, FDR = 0.00009], Itgae [FC = −2.54 FDR = 0.0044]) and the autophagy gene IRGM (FC = −1.94, FDR = 0.01), a recently identified susceptibility gene in human IBD. Consistent with a marked reduction in integrins, probiotic treatment decreased the number of CCL5+ CD3+ double‐positive T cells and upregulated galectin2, which triggers apoptosis of activated T cells. Importantly, genes associated with lipid and PPAR signaling (PPAR&agr; [FC = 2.36, FDR = 0.043], PPARGC1&agr; [FC = 2.58, FDR = 0.016], Nr1d2 [FC = 3.11, FDR = 0.0067]) were also upregulated. Altered microbial diversity was noted in probiotic‐treated mice. Conclusions: Bioinformatics analysis revealed important immune response, phagocytic and inflammatory pathways dominated by elevation of T‐helper cell 1 type (TH1) transcription factors in IL10‐KO mice. Probiotic intervention resulted in a site‐specific reduction of these pathways but importantly upregulated PPAR, xenobiotic, and lipid signaling genes, potential antagonists of NF‐&kgr;B inflammatory pathways. (Inflamm Bowel Dis 2009)
From Glosten-Milgrom to the Whole Limit Order Book and Applications to Financial Regulation

We build an agent-based model for the order book with three types of market participants: informed trader, noise trader and competitive market makers. Using a Glosten-Milgrom like approach, we are able to deduce the whole limit order book (bid-ask spread and volume available at each price) from the interactions between the different agents. More precisely, we obtain a link between efficient price dynamic, proportion of trades due to the noise trader, traded volume, bid-ask spread and equilibrium limit order book state. With this model, we provide a relevant tool for regulators and market platforms. We show for example that it allows us to forecast consequences of a tick size change on the microstructure of an asset. It also enables us to value quantitatively the queue position of a limit order in the book.
Incidence of stroke in people with Alzheimer disease

Objective: Stroke increases the risk of dementias, including Alzheimer disease (AD), but it is unknown whether persons with AD have a higher risk of strokes. We investigated whether noninstitutionalized persons with AD were more likely to experience incident stroke than persons without AD and whether there are differences in the incidence of ischemic or hemorrhagic strokes. Methods: We performed a register-based matched cohort study including all community-dwelling persons with verified clinical diagnosis of AD, residing in Finland on December 31, 2005, and a single age-, sex-, and region of residence–matched comparison person without AD for each individual with AD (n = 56,186, mean age 79.6 [SD 6.9] years). Persons with previous strokes and their matched participants were excluded, leaving 50,808 individuals with 2,947 incident strokes occurring between January 1, 2006, and December 31, 2009. Diagnosis of AD was based on prescription reimbursement register and diagnosis of stroke on hospital discharge register of Finland. Results: AD dementia was not associated with risk of all strokes or ischemic strokes, but the risk of hemorrhagic strokes was higher among persons with AD (adjusted hazard ratio [95% confidence interval] 1.34 [1.12–1.61]). When the associations were analyzed according to age groups, AD was associated with higher risk of all strokes, regardless of etiology, in the 2 youngest age groups, but not in the older groups. Similar associations were observed when the results were categorized according to age at diagnosis. Conclusions: Our findings suggest that persons with AD dementia, especially younger patients, have higher risk of hemorrhagic strokes.
Protective Effects of the Third Generation Vasodilatory Βeta - Blocker Nebivolol against D-Galactosamine - Induced Hepatorenal Syndrome in Rats

BACKGROUND: Renal dysfunction is very common in patients with advanced liver cirrhosis and portal hypertension. The development of renal failure in the absence of clinical, anatomical or pathological causes renal of failure is termed hepatorenal syndrome (HRS). AIM: The present study was constructed to investigate the possible protective effects of nebivolol (Nebi) against D-galactosamine (Gal)-induced HRS in rats. MATERIAL AND METHODS: Rats were treated with Nebi for ten successive days. On the 8th day of the experiment, they received a single dose of Gal. Serum levels of Cr, BUN, Na+ and K+ as well as AST, ALT, total bilirubin (TB), NH3 and endothelin-1 (ET-1) were determined following Gal administration. Moreover, renal and liver contents of MDA, GSH, F2-isoprostanes (F2-IPs), tumor necrosis factor-alpha (TNF-α), nuclear factor kappa-B (NF-κB), total nitric oxide (NO), in addition to activities of caspase-3 (Cas-3), heme oxygenase-1 (HO-1), inducible and endothelial NO synthase (iNOS and eNOS) enzymes were also assessed. Finally, histopathological examination was performed. RESULTS: Nebi attenuated Gal-induced renal and hepatic dysfunction. It also decreased the Gal-induced oxidative stress and inflammatory recruitment. CONCLUSION: Results demonstrated both nephroprotective and hepatoprotective effects of Nebi against HRS and suggested a role of its antioxidant, anti-inflammatory, anti-apoptotic and NO-releasing properties.
The development of a carbon footprint model for the calculation of GHG emissions from highways: the case of Egnatia Odos in Greece

Abstract Global transport demand is increasing and the associated emissions of GHGs are becoming a key factor in the environmental planning of networks and the actual operational management stage. We describe the development of a novel methodology for the calculation of the carbon footprint of a major motorway (Egnatia Odos) in Northern Greece. Total GHG emissions were calculated for 2014 as the base year, from all corporate activities, including stationary and mobile combustion, fugitive gases, purchased electricity, personnel travel, waste disposal and contractor (third party) emissions. End user vehicle emissions constitute a significant part of the carbon footprint and are estimated from annual traffic data supplied by Egnatia Odos S.A. , combined with emission factors extracted from the TREMOVE model, for different vehicle categories and fuel types. The emissions model developed uses additional input data, concerning fuel and electricity consumption, fugitive gases from a/c equipment, personnel commuting and travel, waste disposal, and contractor data, also provided by Egnatia Odos S.A. , for the calculation of direct and indirect GHG emissions for all three Scopes of the GHG Protocol. The final product was developed in the form of a specialized electronic platform, which is user-friendly and can be updated with the most recent input data available, in order to be used by highways’ personnel for the calculation of their carbon footprint in future years. The overall carbon footprint of Egnatia Odos S.A. in 2014 has been estimated at 770 ktCO2e, with 91% of emissions sourced by the end user category (i.e. vehicle emissions).
"Who am I? Why am I here?": self-esteem, self-clarity, and prototype matching.

Recent research has demonstrated that individuals with low self-esteem lack self-clarity; they have less certain and less stable self-concepts than do those with high self-esteem (A. H. Baumgardner, 1990; J. Campbell, 1990). Self-concept confusion should mitigate against the use of a decision-making strategy that involves using the self to guide choice behavior (i.e., prototype matching, P. M. Niedenthal, N. Cantor, & J. F. Kihlstrom, 1985). Two correlational studies demonstrated that people with high self-esteem, but not low self-esteem, made use of prototype matching in forming preferences. In a 3rd study, the self-concept was made more clear or made more confused. Clarity was associated with the use of prototype matching regardless of level of self-esteem. Self-concept confusion was associated with a failure to use the strategy regardless of level of self-esteem.
Phosphorylation of RS1 (RSC1A1) Steers Inhibition of Different Exocytotic Pathways for Glucose Transporter SGLT1 and Nucleoside Transporter CNT1, and an RS1-Derived Peptide Inhibits Glucose Absorption

Cellular uptake adapts rapidly to physiologic demands by changing transporter abundance in the plasma membrane. The human gene RSC1A1 codes for a 67-kDa protein named RS1 that has been shown to induce downregulation of the sodium-D-glucose cotransporter 1 (SGLT1) and of the concentrative nucleoside transporter 1 (CNT1) in the plasma membrane by blocking exocytosis at the Golgi. Injecting RS1 fragments into Xenopus laevis oocytes expressing SGLT1 or CNT1 and measuring the expressed uptake of α-methylglucoside or uridine 1 hour later, we identified a RS1 domain (RS1-Reg) containing multiple predicted phosphorylation sites that is responsible for this post-translational downregulation of SGLT1 and CNT1. Dependent on phosphorylation, RS1-Reg blocks the release of SGLT1-containing vesicles from the Golgi in a glucose-dependent manner or glucose-independent release of CNT1-containing vesicles. We showed that upregulation of SGLT1 in the small intestine after glucose ingestion is promoted by glucose-dependent disinhibition of the RS1-Reg–blocked exocytotic pathway of SGLT1 between meals. Mimicking phosphorylation of RS1-Reg, we obtained a RS1-Reg variant that downregulates SGLT1 in the brush-border membrane at high luminal glucose concentration. Because RS1 mediates short-term regulation of various transporters, we propose that the RS1-Reg–navigated transporter release from Golgi represents a basic regulatory mechanism of general importance, which implies the existence of receptor proteins that recognize different phosphorylated forms of RS1-Reg and of complex transporter-specific sorting in the trans-Golgi. RS1-Reg–derived peptides that downregulate SGLT1 at high intracellular glucose concentrations may be used for downregulation of glucose absorption in small intestine, which has been proposed as strategy for treatment of type 2 diabetes.
Novel Munc13–4 mutations in children and young adult patients with haemophagocytic lymphohistiocytosis

Familial haemophagocytic lymphohistiocytosis (FHL) is a genetically heterogeneous disorder characterised by constitutive defects in cellular cytotoxicity resulting in fever, hepatosplenomegaly and cytopenia, and the outcome is fatal unless treated by chemoimmunotherapy followed by haematopoietic stem-cell transplantation. Since 1999, mutations in the perforin gene giving rise to this disease have been identified; however, these account only for 40% of cases. Lack of a genetic marker hampers the diagnosis, suitability for transplantation, selection of familial donors, identification of carriers, genetic counselling and prenatal diagnosis. Mutations in the Munc13–4 gene have recently been described in patients with FHL. We sequenced the Munc13–4 gene in all patients with haemophagocytic lymphohistiocytosis not due to PRF1 mutations. In 15 of the 30 families studied, 12 novel and 4 known Munc13–4 mutations were found, spread throughout the gene. Among novel mutations, 2650C→T introduced a stop codon; 441del A, 532del C, 3082del C and 3226ins G caused a frameshift, and seven were mis sense mutations. Median age of diagnosis was 4 months, but six patients developed the disease after 5 years of age and one as a young adult of 18 years. Involvement of central nervous system was present in 9 of 15 patients, activity of natural killer cells was markedly reduced or absent in 13 of 13 tested patients. Chemo-immunotherapy was effective in all patients. Munc13–4 mutations were found in 15 of 30 patients with FHL without PRF1 mutations. Because these patients may develop the disease during adolescence or even later, haematologists should include FHL2 and FHL3 in the differential diagnosis of young adults with fever, cytopenia, splenomegaly and hypercytokinaemia.
Parathyroid hormone is associated with the LV mass after aortic valve replacement

Aims LV hypertrophy (LVH) is frequent after aortic valve replacement (AVR) and is often associated with comorbidities, including hypertension, obesity, renal failure and prosthesis-patient mismatch (PPM). However, whether other biological mechanism(s) may participate to LVH after AVR is still unknown. Parathyroid hormone (PTH) may play a role in LVH. However, it is presently unknown whether PTH is associated with LVH in patients that have undergone an AVR. Methods In this cross-sectional study, 195 patients have been investigated at a mean of 8±3.5 years following AVR. LV function and mass were evaluated by Doppler echocardiography. The plasma levels of PTH, 25-hydroxyvitamin D (25-OHD), calcium and phosphate were measured. Results There were 102 (52%) patients with LVH after AVR. In univariate analyses, PTH blood level was associated with LV mass (LVMi) and LVH. After adjustment for other risk factors, elevated PTH remained associated with LVMi (p=0.003) and LVH (p=0.02). In turn, the blood levels of 25-OHD and the renal function (GFR) were independently and inversely related to the blood level of PTH. Conclusions After AVR, the level of PTH is independently associated with LVH. In turn, the level of PTH is related with the renal function and the level of 25-OHD.
DnaA protein interacts with RNA polymerase and partially protects it from the effect of rifampicin

The Escherichia coli DnaA protein forms an oligomer at the origin and initiates chromosome replication with the aid of architectural elements and transcription by RNA polymerase. Rifampicin inhibits initiation of transcription by RNA polymerase and thus also initiation of replication. Here, we report that wild‐type cells undergo rifampicin‐resistant initiation of replication during slow growth in acetate medium. The rifampicin‐resistant initiation was prevented by reducing the availability of DnaA. In vitro experiments showed that the DnaA protein interacted with RNA polymerase and that it afforded a partial protection from the negative effect of rifampicin. It is possible that rifampicin‐resistant rounds of replication occur when a surplus of DnaA is available at the origin. In rich medium wild‐type cells do not exhibit rifampicin‐resistant rounds of replication, possibly indicating that there is no surplus DnaA, and that DnaA activity is the factor limiting the process of initiation. During growth in acetate medium, on the contrary, DnaA activity is not limiting in the same way because an initiation potential is present and can be turned into extra rounds of replication when rifampicin is added. The result suggests that regulation of replication initiation may differ at different growth rates.
Outcomes of Pure Laparoscopic versus Open Hepatic Resection for Hepatocellular Carcinoma in Cirrhotic Patients: A Case-Control Study with Propensity Score Matching

Background/Purpose: Laparoscopic hepatic resection (LH) for hepatocellular carcinoma (HCC) has gradually gained ground as a safe and minimally invasive treatment, although LH for cirrhotic patients remains challenging. Methods: Between January 2007 and August 2014, 28 and 57 patients with histologically proven cirrhosis (histological activity index, fibrosis score 4) underwent pure LH and open hepatic resection (OH; less than segmentectomy), respectively, for peripheral HCC ≤5 cm. To correct the difference in clinicopathological factors, including difficulty scores, between the two groups, propensity score matching was used at a 1:1 ratio, which resulted in a comparison of 20 patients per group. We compared the short- and long-term outcomes of LH and OH to investigate the efficacy of LH. Results: Clinicopathological variables, including difficulty scores, were well balanced between the two groups. The incidence of complications and mean intraoperative blood loss were lower in the LH group than the OH group (0 vs. 45% and 180 vs. 440 ml, p = 0.001 and 0.04, respectively). The 3-year disease-free survival rate was 42% in the LH group and 30% in the OH group (p = 0.533), whereas the 5-year overall survival rates were 46 and 60%, respectively (p = 0.606). Conclusions: LH is a safe and effective treatment option for cirrhotic patients with HCC in terms of intraoperative blood loss and morbidity.
High-density lipoprotein as a therapeutic target: a systematic review.

CONTEXT High-density lipoprotein cholesterol (HDL-C) is a cardiovascular risk factor that is gaining substantial interest as a therapeutic target. OBJECTIVES To review the current and emerging strategies that modify high-density lipoproteins (HDLs). DATA SOURCES Systematic search of English-language literature (1965-May 2007) in MEDLINE and the Cochrane database, using the key words HDL-C and apolipoprotein A-I and the subheadings reverse cholesterol transport, CVD [cardiovascular disease] prevention and control, drug therapy, and therapy; review of presentations made at major cardiovascular meetings from 2003-2007; and review of ongoing trials from ClinicalTrials.gov and current guidelines from major cardiovascular societies. STUDY SELECTION AND DATA EXTRACTION Study selection was prioritized to identify randomized controlled trials over meta-analyses over mechanistic studies; identified studies also included proof-of-concept studies and key phase 1 through 3 trials of novel agents. Study eligibility was assessed by 2 authors; disagreements were resolved by consensus with the third. DATA SYNTHESIS Of 754 studies identified, 31 randomized controlled trials met the inclusion criteria. Currently available therapeutic and lifestyle strategies, when optimized, increase HDL-C levels by 20% to 30%. While basic and small pilot studies have shown promise, proof that increasing HDL-C levels confers a reduction in major cardiovascular outcomes independent of changes in levels of low-density lipoprotein cholesterol or triglycerides has been more elusive. Some novel therapeutic agents in human studies appear to effectively increase HDL-C levels, whereas other novel strategies that target HDL metabolism or function may have minimal effect on HDL-C levels. CONCLUSIONS At present there is modest evidence to support aggressively increasing HDL-C levels in addition to what is achieved by lifestyle modification alone. Ongoing clinical trials that target specific pathways in HDL metabolism may help expand cardiovascular treatment options.
Influence of anesthetic agent, depth of anesthesia and body temperature on cardiovascular functional parameters in the rat

Sedating animals is sometimes necessary in experimental research. This paper presents and discusses the influence of four of the most common anesthetic agents on cardiovascular parameters in rats. We also studied the influence of body temperature. Ten-week-old Sprague-Dawley rats were anesthetized with either isoflurane, pentobarbital, ketamine/xylazine or tiletamine/zolazepam (n = 12 in each group). A pressure-sensing catheter was placed in the right carotid artery for the continuous measurement of arterial pressure, and echocardiography was performed. Indices of cardiac function were significantly higher in the tiletamine/zolazepam rats compared with the other groups. Heart rate was highest but stroke volume lowest with pentobarbital. Left ventricular diastolic dimension was lower in the pentobarbital and tiletamine/zolazepam rats compared with the isoflurane or ketamine/xylazine rats. Intraventricular diastolic pressure was similar in all groups whereas intraventricular systolic pressure, as well as both systolic and diastolic aortic pressures, was significantly higher in the tiletamine/zolazepam rats compared with the other groups. No hemodynamic indices differed significantly among the isoflurane, pentobarbital and ketamine/xylazine rats. Lowering body temperature significantly reduced heart rate and cardiac output but had no apparent effect on hemodynamic parameters. In conclusion, although cardiac functional parameters differed between the different anesthetic agents in ways that could be of relevance to the researcher, they may all have a role in experimental cardiology. Importantly, tiletamine/zolazepam anesthesia resulted in significantly higher indices of cardiac function and elevated blood pressures compared with the other anesthetic agents, a finding that should be kept in mind when interpreting data obtained in rats sedated on this regimen.