bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of stearidonic acid-enriched soybean oil on fatty acid profile and metabolic parameters in lean and obese Zucker rats
Authors: Casey John M , Banz William J , Krul Elaine S , Butteiger Dustie N , Goldstein Daniel A , Davis Jeremy E 
Published: October 2013

Abstract

Background
Consumption of marine-based oils high in omega-3 polyunsaturated fatty acids (n3PUFAs), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) is known to protect against obesity-related pathologies. It is less clear whether traditional vegetable oils with high omega-6 polyunsaturated fatty acid (n6PUFA) content exhibit similar therapeutic benefits. As such, this study examined the metabolic effects of a plant-based n3PUFA, stearidonic acid (SDA), in polygenic obese rodents.

Methods
Lean (LZR) and obese Zucker (OZR) rats were provided either a standard westernized control diet (CON) with a high n6PUFA to n3PUFA ratio (i.e., 16.2/1.0) or experimental diet modified with flaxseed (FLAX), menhaden (FISH), or SDA oil that resulted in n6PUFA to n3PUFA ratios of 1.7/1.0, 1.3/1.0, and 1.0/0.8, respectively.

Results
After 12 weeks, total adiposity, dyslipidemia, glucose intolerance, and hepatic steatosis were all greater, whereas n3PUFA content in liver, adipose, and muscle was lower in OZR vs. LZR rats. Obese rodents fed modified FISH or SDA diets had lower serum lipids and hepatic fat content vs. CON. The omega-3 index (i.e., ΣEPA + DHA in erythrocyte membrane) was 4.0, 2.4, and 2.0-fold greater in rodents provided FISH, SDA, and FLAX vs. CON diet, irrespective of genotype. Total hepatic n3PUFA and DHA was highest in rats fed FISH, whereas both hepatic and extra-hepatic EPA was higher with FISH and SDA groups.

Conclusions
These data indicate that SDA oil represents a viable plant-derived source of n3PUFA, which has therapeutic implications for several obesity-related pathologies.
Pulmonary benign metastasizing leiomyoma: report of three cases
Authors: Jeon Hyun Woo , Choi Soo Hwan , Sung Sook Whan , Park Jae Kil 
Published: October 2013

Abstract
Benign metastasizing leiomyoma is very rare and usually occurs in women who undergo hysterectomy and myomectomy for uterine leiomyoma. This is a benign spindle-shaped smooth muscle cell tumor pathologically but metastasizes to the extrauterine organs. Lungs are the most common site of metastasis. We observed three cases of pulmonary benign metastasizing leiomyoma.
Assessing communities of practice in health policy: a conceptual framework as a first step towards empirical research
Authors: Bertone Maria Paola , Meessen Bruno , Clarysse Guy , Hercot David , Kelley Allison , Kafando Yamba , Lange Isabelle , Pfaffmann Jérôme , Ridde Valéry , Sieleunou Isidore , Witter Sophie 
Published: October 2013

Abstract
Communities of Practice (CoPs) are groups of people that interact regularly to deepen their knowledge on a specific topic. Thanks to information and communication technologies, CoPs can involve experts distributed across countries and adopt a ‘transnational’ membership. This has allowed the strategy to be applied to domains of knowledge such as health policy with a global perspective. CoPs represent a potentially valuable tool for producing and sharing explicit knowledge, as well as tacit knowledge and implementation practices. They may also be effective in creating links among the different ‘knowledge holders’ contributing to health policy (e.g., researchers, policymakers, technical assistants, practitioners, etc.).
CoPs in global health are growing in number and activities. As a result, there is an increasing need to document their progress and evaluate their effectiveness. This paper represents a first step towards such empirical research as it aims to provide a conceptual framework for the analysis and assessment of transnational CoPs in health policy.
The framework is developed based on the findings of a literature review as well as on our experience, and reflects the specific features and challenges of transnational CoPs in health policy. It organizes the key elements of CoPs into a logical flow that links available resources and the capacity to mobilize them, with knowledge management activities and the expansion of knowledge, with changes in policy and practice and, ultimately, with an improvement in health outcomes. Additionally, the paper addresses the challenges in the operationalization and empirical application of the framework.
Comprehensive analysis of the percentage of surface receptors and cytotoxic granules positive natural killer cells in patients with pancreatic cancer, gastric cancer, and colorectal cancer
Authors: Peng Yun-Peng , Zhu Yi , Zhang Jing-Jing , Xu Ze-Kuan , Qian Zhu-Yin , Dai Cun-Cai , Jiang Kui-Rong , Wu Jun-Li , Gao Wen-Tao , Li Qiang , Du Qing , Miao Yi 
Published: October 2013

AbstractBackgroundDigestive malignancies, especially pancreatic cancer (PC), gastric cancer (GC), and colorectal cancer (CRC), still occur at persistently high rates, and disease progression in these cancers has been associated with tumor immunosurveillance escape. Natural killer (NK) cell dysfunction may be responsible for this phenomenon, however, the exact relationship between tumor immunosurveillance escape in digestive malignancies and NK cell dysfunction remains unclear.MethodsPercentage of the surface receptors NKG2A, KIR3DL1, NKG2D, NKp30, NKp44, NKp46, and DNAM-1, as well as the cytotoxic granules perforin and granzyme B positive NK cells were determined in patients with pancreatic cancer (n = 31), gastric cancer (n = 31), and CRC (n = 32) prior to surgery and healthy controls (n = 31) by multicolor flow cytometry. Independentt-tests or Mann-Whitney U-tests were used to compare the differences between the patient and healthy control groups, as well as the differences between patients with different pathologic features of cancer.ResultsPercentage of NKG2D, NKp30, NKp46, and perforin positive NK cells was significantly down-regulated in patients with PC compared to healthy controls, as well as GC and CRC; reduced levels of these molecules was associated with indicators of disease progression in each malignancy (such as histological grade, depth of invasion, lymph node metastasis). On the contrary, percentage of KIR3DL1 positive NK cells was significantly increased in patients with PC, as well as GC and CRC, but was not associated with any indicators of disease progression.ConclusionsAltered percentage of surface receptors and cytotoxic granules positive NK cells may play a vital role in tumor immunosurveillance escape by inducing NK cell dysfunction in patients with PC, GC, and CRC.
Preserved endothelial function in human obesity in the absence of insulin resistance
Authors: El Assar Mariam , Ruiz de Adana Juan Carlos , Angulo Javier , Pindado Martínez María Luz , Hernández Matías Alberto , Rodríguez-Mañas Leocadio 
Published: October 2013

Abstract

Background
Insulin resistance (IR) is frequently associated with endothelial dysfunction and has been proposed to play a major role in cardiovascular disease (CVD). On the other hand, obesity has long been related to IR and increased CVD. However it is not known if IR is a necessary condition for endothelial dysfunction in human obesity, allowing for preserved endothelial function in obese people when absent. Therefore, the purpose of the study was to assess the relationship between IR and endothelial dysfunction in human obesity and the mechanisms involved.

Methods
Twenty non-insulin resistant morbid obese (NIR-MO), 32 insulin resistant morbid obese (IR-MO), and 12 healthy subjects were included. Serum concentrations of glucose, insulin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), resistin and adiponectin were determined. IR was evaluated by HOMA-index. Endothelium-dependent relaxation to bradykinin (BK) in mesenteric microvessels was assessed in wire myograph.

Results
Serum IL-6, and TNF-α levels were elevated only in IR-MO patients while resistin was elevated and adiponectin reduced in all MO individuals. Mesenteric arteries from IR-MO, but not from NIR-MO subjects displayed blunted relaxation to BK. Vasodilatation was improved in IR-MO arteries by the superoxide scavenger, superoxide dismutase (SOD) or the mitochondrial-targeted SOD mimetic, mito-TEMPO. NADPH oxidase inhibitors (apocynin and VAS2870) and the nitric oxide synthase (NOS) cofactor, tetrahydrobiopterin failed to modify BK-induced vasodilatations. Superoxide generation was higher in vessels from IR-MO subjects and reduced by mito-TEMPO. Blockade of TNF-α with infliximab, but not inhibition of inducible NOS or cyclooxygenase, improved endothelial relaxation and decreased superoxide formation.

Conclusions
Endothelial dysfunction is observed in human morbid obesity only when insulin resistance is present. Mechanisms involved include augmented mitochondrial superoxide generation, and increased systemic inflammation mediated by TNF-α. These findings may explain the different vascular risk of healthy vs unhealthy obesity.
Polydatin, a natural precursor of resveratrol, induces cell cycle arrest and differentiation of human colorectal Caco-2 cell
Authors: De Maria Salvatore , Scognamiglio Ilaria , Lombardi Angela , Amodio Nicola , Caraglia Michele , Cartenì Maria , Ravagnan Gianpietro , Stiuso Paola 
Published: October 2013

Abstract

Background
Human colon adenocarcinoma cells are resistant to chemotherapeutic agents, such as anthracyclines, that induce death by increasing the reactive oxygen species. A number of studies have been focused on chemo-preventive use of resveratrol as antioxidant against cardiovascular diseases, aging and cancer. While resveratrol cytotoxic action was due to its pro-oxidant properties. In this study, we investigate whether the Resveratrol (trans-3,5,49-trihydroxystilbene) and its natural precursor Polydatin (resveratrol-3-O-b-mono- D-glucoside, the glycoside form of resveratrol) combination, might have a cooperative antitumor effect on either growing or differentiated human adenocarcinoma colon cancer cells.

Methods
The polydatin and resveratrol pharmacological interaction was evaluated in vitro on growing and differentiated Caco-2 cell lines by median drug effect analysis calculating a combination index with CalcuSyn software. We have selected a synergistic combination and we have evaluated its effect on the biological and molecular mechanisms of cell death.

Results
Simultaneous exposure to polydatin and resveratrol produced synergistic antiproliferative effects compared with single compound treatment. We demonstrated that polydatin alone or in combination with resveratrol at 3:1 molar ratio synergistically modulated oxidative stress, cell cycle, differentiation and apoptosis. Worthy of note treatment with polydatin induced a nuclear localization and decreased expression of heat shock protein 27, and vimentin redistributed within the cell.

Conclusions
From morphological, and biochemical outcome we obtained evidences that polydatin induced a transition from a proliferative morphology to cell-specific differentiated structures and caused human CaCo-2 cell death by induction of apoptosis. Our data suggest the potential use of polydatin in combination chemotherapy for human colon cancer.
A mathematical model for optimizing the indications of liver transplantation in patients with hepatocellular carcinoma
Authors: Chaib Eleazar , Amaku Marcos , Coutinho Francisco AB , Lopez Luis F , Burattini Marcelo N , D’Albuquerque Luiz AC , Massad Eduardo 
Published: October 2013

Abstract

Background
The criteria for organ sharing has developed a system that prioritizes liver transplantation (LT) for patients with hepatocellular carcinoma (HCC) who have the highest risk of wait-list mortality. In some countries this model allows patients only within the Milan Criteria (MC, defined by the presence of a single nodule up to 5 cm, up to three nodules none larger than 3 cm, with no evidence of extrahepatic spread or macrovascular invasion) to be evaluated for liver transplantation. This police implies that some patients with HCC slightly more advanced than those allowed by the current strict selection criteria will be excluded, even though LT for these patients might be associated with acceptable long-term outcomes.

Methods
We propose a mathematical approach to study the consequences of relaxing the MC for patients with HCC that do not comply with the current rules for inclusion in the transplantation candidate list. We consider overall 5-years survival rates compatible with the ones reported in the literature. We calculate the best strategy that would minimize the total mortality of the affected population, that is, the total number of people in both groups of HCC patients that die after 5 years of the implementation of the strategy, either by post-transplantation death or by death due to the basic HCC. We illustrate the above analysis with a simulation of a theoretical population of 1,500 HCC patients with tumor size exponentially. The parameter λ obtained from the literature was equal to 0.3. As the total number of patients in these real samples was 327 patients, this implied in an average size of 3.3 cm and a 95% confidence interval of [2.9; 3.7]. The total number of available livers to be grafted was assumed to be 500.

Results
With 1500 patients in the waiting list and 500 grafts available we simulated the total number of deaths in both transplanted and non-transplanted HCC patients after 5 years as a function of the tumor size of transplanted patients. The total number of deaths drops down monotonically with tumor size, reaching a minimum at size equals to 7 cm, increasing from thereafter. With tumor size equals to 10 cm the total mortality is equal to the 5 cm threshold of the Milan criteria.

Conclusion
We concluded that it is possible to include patients with tumor size up to 10 cm without increasing the total mortality of this population.
Median ages at stages of sexual maturity and excess weight in school children
Authors: Luciano Alexandre P , Benedet Jucemar , de Abreu Luiz Carlos , Valenti Vitor E , de Souza Almeida Fernando , de Vasconcelos Francisco AG , Adami Fernando 
Published: October 2013

AbstractBackgroundWe aimed to estimate the median ages at specific stages of sexual maturity stratified by excess weight in boys and girls.Materials and methodThis was a cross-sectional study made in 2007 in Florianopolis, Brazil, with 2,339 schoolchildren between 8 to 14 years of age (1,107 boys) selected at random in two steps (by region and type of school). The schoolchildren were divided into: i) those with excess weight and ii) those without excess weight, according to the WHO 2007 cut-off points for gender and age. Sexual maturity was self-evaluated by the subjects according to the Tanner sexual development stages, and utilizing median ages for the genitalia, breasts, and pubic hair stages.ResultsIn the boys with excess weight, precocity was observed in the stages 4 for genitals and pubic hair and 2 for pubic hair, with the values for excess and normal weight. The median ages at the beginning of puberty (stage 2–sexual development) for boys and girls in Florianopolis were 10.8 and 10.3 years, respectively.ConclusionExcess weight is associated with lower median ages in the sexual maturity stages in boys and girls and that it should be taken into account when evaluating sexual maturity in children and adolescents.
Novel ω-Conotoxins from C. Catus Reverse Signs of Mouse Inflammatory Pain after Systemic Administration
Authors: Sadeghi Mahsa , Murali Swetha S , Lewis Richard J , Alewood Paul F , Mohammadi Sarasa , Christie MacDonald J 
Published: October 2013

Background Antagonists of N-type voltage-gated calcium channels (VGCC), Cav2.2, can manage severe chronic pain with intrathecal use and may be effective systemically. A series of novel ω-conotoxins that selectively inhibit N-type VGCCs was isolated from Conus catus. In the present study, the potency and reversibility of ω-conotoxins CVID, CVIE and CVIF to inhibit N-type calcium currents were investigated in mouse isolated dorsal root ganglion (DRG) neurons. The systemic potency of each ω-conotoxin to reverse signs of mouse chronic inflammatory pain was also compared. Results In DRG neurons, the rank order of potency to inhibit N-type calcium currents was CVIE > CVIF > CVID. After subcutaneous administration, CVID and CVIE, but not CVIF, partially reversed impaired weight bearing in mice injected with Freund's complete adjuvant (CFA) three days prior to testing. No side-effects associated with systemic administration of ω-conotoxins were observed. Conclusions The present study indicates a potential for CVID and CVIE to be developed as systemically active analgesics with no accompanying neurological side-effects.
Method to grow Actinobacillus pleuropneumoniaebiofilm on a biotic surface
Authors: Tremblay Yannick DN , Lévesque Cynthia , Segers Ruud PAM , Jacques Mario 
Published: October 2013

Abstract

Background

Actinobacillus pleuropneumoniae is a Gram-negative bacterium and a member of the Pasteurellaceae family. This bacterium is the causative agent of porcine pleuropneumonia, which is a highly contagious respiratory disease causing important economical losses to the worldwide pig industry. It has been shown that A. pleuropneumoniae can form biofilms on abiotic surfaces (plastic and glass). Although in vitro models are extremely useful to gain information on biofilm formation, these models may not be representative of the conditions found at the mucosal surface of the host, which is the natural niche of A. pleuropneumoniae.

Results
In this paper, we describe a method to grow A. pleuropneumoniae biofilms on the SJPL cell line, which represents a biotic surface. A non-hemolytic, non-cytotoxic mutant of A. pleuropneumoniae was used in our assays and this allowed the SJPL cell monolayers to be exposed to A. pleuropneumoniae for longer periods. This resulted in the formation of biofilms on the cell monolayer after incubations of 24 and 48 h. The biofilms can be stained with fluorescent probes, such as a lectin against the polymer of N-acetyl-D-glucosamine present in the biofilm matrix, and easily observed by confocal laser scanning microscopy.

Conclusions
This is the first protocol that describes the formation of an A. pleuropneumoniae biofilm on a biotic surface. The advantage of this protocol is that it can be used to study biofilm formation in a context of host-pathogen interactions. The protocol could also be adapted to evaluate biofilm inhibitors or the efficacy of antibiotics in the presence of biofilms.
GPI-anchor and GPI-anchored protein expression in PMM2-CDG patients
Authors: de la Morena-Barrio Maria E , Hernández-Caselles Trinidad , Corral Javier , García-López Roberto , Martínez-Martínez Irene , Pérez-Dueñas Belen , Altisent Carmen , Sevivas Teresa , Kristensen Soren R , Guillén-Navarro Encarna , Miñano Antonia , Vicente Vicente , Jaeken Jaak , Lozano Maria L 
Published: October 2013

AbstractBackgroundMutations inPMM2impair phosphomannomutase-2 activity and cause the most frequent congenital disorder of glycosylation, PMM2-CDG. Mannose-1-phosphate, that is deficient in this disorder, is also implicated in the biosynthesis of glycosylphosphatidyl inositol (GPI) anchors.ObjectiveTo evaluate whether GPI-anchor and GPI-anchored proteins are defective in PMM2-CDG patients.MethodsThe expression of GPI-anchor and seven GPI-anchored proteins was evaluated by flow cytometry in different cell types from twelve PMM2-CDG patients. Additionally, neutrophil CD16 and plasma hepatic proteins were studied by Western blot. Transferrin glycoforms were evaluated by HPLC.ResultsPatients and controls had similar surface expression of GPI-anchor and most GPI-anchored proteins. Nevertheless, patients displayed a significantly diminished binding of two anti-CD16 antibodies (3G8 and KD1) to neutrophils and also of anti-CD14 (61D3) to monocytes. Interestingly, CD16 immunostaining and asialotransferrin levels significantly correlated with patients’ age. Analysis by flow cytometry of CD14 with MΦP9, and CD16 expression in neutrophils by Western blot using H-80 ruled out deficiencies of these antigens.ConclusionsPMM2mutations do not impair GPI-anchor or GPI-anchored protein expression. However, the glycosylation anomalies caused byPMM2mutations might affect the immunoreactivity of monoclonal antibodies and lead to incorrect conclusions about the expression of different proteins, including GPI-anchored proteins. Neutrophils and monocytes are sensitive toPMM2mutations, leading to abnormal glycosylation in immune receptors, which might potentially affect their affinity to their ligands, and contribute to infection. This study also confirms less severe hypoglycosylation defects in older PMM2-CDG patients.
Endogenous expression of FAD-linked PS1 impairs proliferation, neuronal differentiation and survival of adult hippocampal progenitors
Authors: Veeraraghavalu Karthikeyan , Choi Se Hoon , Zhang Xiaoqiong , Sisodia Sangram S 
Published: October 2013

Abstract

Background
Alzheimer’s disease (AD) is characterized by progressive memory loss and impaired cognitive function. Early-onset familial forms of the disease (FAD) are caused by inheritance of mutant genes encoding presenilin 1 (PS1) variants. We have demonstrated that prion promoter (PrP)-driven expression of human FAD-linked PS1 variants in mice leads to impairments in environmental enrichment (EE)-induced adult hippocampal neural progenitor cell (AHNPC) proliferation and neuronal differentiation, and have provided evidence that accessory cells in the hippocampal niche expressing PS1 variants may modulate AHNPC phenotypes, in vivo. While of significant interest, these latter studies relied on transgenic mice that express human PS1 variant transgenes ubiquitously and at high levels, and the consequences of wild type or mutant PS1 expressed under physiologically relevant levels on EE-mediated AHNPC phenotypes has not yet been tested.

Results
To assess the impact of mutant PS1 on EE-induced AHNPC phenotypes when expressed under physiological levels, we exposed adult mice that constitutively express the PSEN1 M146V mutation driven by the endogenous PSEN1 promoter (PS1 M146V “knock-in” (KI) mice) to standard or EE-housed conditions. We show that in comparison to wild type PS1 mice, AHNPCs in mice carrying homozygous (PS1

M146V/M146V
) or heterozygous (PS1

M146V/+
) M146V mutant alleles fail to exhibit EE-induced proliferation and commitment towards neurogenic lineages. More importantly, we report that the survival of newborn progenitors are diminished in PS1 M146V KI mice exposed to EE-conditions compared to respective EE wild type controls.

Conclusions
Our findings reveal that expression at physiological levels achieved by a single PS1 M146V allele is sufficient to impair EE-induced AHNPC proliferation, survival and neuronal differentiation, in vivo. These results and our finding that microglia expressing a single PS1 M146V allele impairs the proliferation of wild type AHNPCs in vitro argue that expression of mutant PS1 in the AHNPC niche impairs AHNPCs phenotypes in a dominant, non-cell autonomous manner.