bluuebunny/crossref_metadata_2025_split huggingface dataset:
Salmonella in meats, water, fruit and vegetables as disclosed from testing undertaken by Food Business Operators in Ireland from 2005 to 2009
Authors: Duggan Sharon , Jordan Emily , Gutierrez Montserrat , Barrett Gaye , O’Brien Tony , Hand Darren , Kenny Kevin , Fanning June , Leonard Nola , Egan John 
Published: September 2012

Abstract
Food Business Operators (FBO) are responsible for the safety of the food they produce and in Ireland those under the regulatory control of the Department of Agriculture, Food and Marine are required to provide summary data on microbiological tests undertaken as part of their food safety controls. These data are provided to the National Reference Laboratory through the 25 private laboratories undertaking the testing.

Results

Over the five-year period Salmonella sp. was isolated from 0.7% of the 254,000 raw meat or raw meat products tested with the annual prevalence ranging from 0.5 to 1.1%. Poultry meats were consistently more contaminated than other meats with higher recovery rates in turkey (3.3%), duck (3.3%), and chicken (2.5%) compared with meats of porcine (1.6%), ovine (0.2%) and bovine origin (0.1%). Salmonella sp. was also isolated from 58 (0.06%) of the 96,115 cooked or partially cooked meat and meat products tested during the reporting period with the annual percentage positive samples ranging from 0.01 to 0.16%. A total of 50 different serotypes were recovered from raw meats over this period with the greatest diversity found in poultry samples (n = 36). Four serotypes, Kentucky, Typhimurium, Agona and Derby accounted for over 70% of all isolates detected on FBO testing over the period 2005 to 2009.

Conclusions

Capturing microbiological data generated by Food Business Operators allows the regulatory sector access to a substantial amount of valuable data with the minimum financial outlay.
Development of an effective risk management system in a teaching hospital
Authors: Adibi Hossein , Khalesi Nader , Ravaghi Hamid , Jafari Mahdi , Jeddian Ali Reza 
Published: September 2012

Abstract
Background
Unsafe health care provision is a main cause of increased mortality rate amongst hospitalized patients all over the world. A system approach to medical error and its reduction is crucial that is defined by clinical and administrative activities undertaken to identify, evaluate, and reduce the risk of injury. The aim of this study was to develop and implement a risk management system in a large teaching hospital in Iran, especially of the basis of WHO guidelines and patient safety context.

Methods
WHO draft guideline and patient safety reports from different countries were reviewed for defining acceptable framework of risk management system. Also current situation of mentioned hospital in safety matter and dimensions of patient safety culture was evaluated using HSOPSC questionnaire of AHRQ. With adjustment of guidelines and hospital status, the conceptual framework was developed and next it was validated in expert panel. The members of expert panel were selected according to their role and functions and also their experiences in risk management and patient safety issues. The validated framework consisted of designating a leader and coordinator core, defining communications, and preparing the infrastructure for patient safety education and culture-building. That was developed on the basis of some values and commitments and included reactive and proactive approaches.

Results
The findings of reporting activities demonstrated that at least 3.6 percent of hospitalized patients have experienced adverse events and 5.3 percent of all deaths in the hospital related with patient safety problems. Beside the average score of 12 dimensions of patient safety culture was 46.2 percent that was considerably low. The “non-punitive responses to error” had lowest positive score with 21.2 percent.

Conclusion
It is of paramount importance for all health organizations to lay necessary foundations in order to identify safety risks and improve the quality of care. Inadequate participation of staff in education, reporting and analyzing, underreporting and uselessness of aggregated data, limitation of human and financial resources, punitive directions and management challenges for solutions were the main executive problems which could affect the effectiveness of system.
Ablation of Leptin Signaling to Somatotropes: Changes in Metabolic Factors that Cause Obesity
Authors: Akhter Noor , Odle Angela K. , Allensworth-James Melody L. , Haney Anessa C. , Syed Mohsin M. , Cozart Michael A. , Chua Streamson , Kineman Rhonda , Childs Gwen V. 
Published: September 2012

AbstractMice with somatotrope-specific deletion of the Janus kinase binding site in leptin receptors are GH deficient as young adults and become obese by 6 months of age. This study focused on the metabolic status of young (3–4.5 month old) preobese mutant mice. These mutants had normal body weights, lean body mass, serum leptin, glucose, and triglycerides. Mutant males and females showed significantly higher respiratory quotients (RQ) and lower energy output, resulting from a higher volume of CO2 output and lower volume of O2 consumption. Deletion mutant females were significantly less active than controls; they had higher levels of total serum ghrelin and ate more food. Mutant females also had lower serum insulin and higher glucagon. In contrast, deletion mutant males were not hyperphagic, but they were more active and spent less time sleeping. Adiponectin and resistin, both products of adipocytes, were increased in male and female mutant mice. In addition, mutant males showed an increase in circulating levels of the potent lipogenic hormone, glucose-dependent insulinotropic peptide. Taken together, these results indicate that mutant mice may become obese due to a reduction in lipid oxidation and energy expenditure. This may stem from GH deficiency. Reduced fat oxidation and enhanced insulin sensitivity (in females) are directly related to GH deficiency in mutant mice because GH has been shown by others to increase insulin sensitivity and fat oxidation and reduce carbohydrate oxidation. Gender-dependent alterations in metabolic signals may further exacerbate the future obese phenotype and affect the timing of its onset. Females show a delay in onset of obesity, perhaps because of their low serum insulin, which is lipogenic, whereas young males already have higher levels of the lipogenic hormone, glucose-dependent insulinotropic peptide. These findings signify that leptin signals to somatotropes are vital for the normal metabolic activity needed to optimize body composition.
Cross Talk between PKC and CREB in the Induction of COX-2 by PGF2α in Human Amnion Fibroblasts
Authors: Guo C. M. , Kasaraneni N. , Sun K. , Myatt L. 
Published: September 2012

AbstractCompelling evidence indicates a crucial role of prostaglandin F2α (PGF2α) in parturition. Both the maternal and fetal sides of the fetal membranes synthesize PGF2α, which exerts effects via the prostaglandin F2α receptor (FP) that is coupled to the activation of protein kinase C (PKC). Cyclooxygenase-2 (COX-2) catalyzes the rate-limiting step of the inducible synthesis of prostaglandin. Although activation of PKC is known to induce COX-2 expression, it is not clear whether PGF2α can induce COX-2 via FP receptor-coupled PKC activation. COX-2 promoter carries a cAMP-response element (CRE) and phosphorylation of CRE binding protein 1 (CREB1) is associated with COX-2 expression in human amnion fibroblasts. We demonstrated that human amnion fibroblasts produced PGF2α and expressed FP receptor. PGF2α increased COX-2 expression and CREB1 phosphorylation, which could be blocked by either the FP receptor antagonist AL8810 or PKC inhibitor Ro31-7549. The PKC activator, phorbol-12-myristate-13-acetate (PMA), could mimic the induction of COX-2 and CREB1 phosphorylation. The induction of COX-2 by PGF2α and PMA could be attenuated by the small interfering RNA-mediated knockdown of CREB1 expression or overexpressing dominant-negative CREB1. A chromatin immunoprecipitation assay showed that the binding of CREB1 to the COX-2 promoter was increased by PGF2α and PMA in amnion fibroblasts. In conclusion, we provide evidence that PGF2α induces COX-2 expression via the FP receptor and phosphorylates CREB1 by PKC, thus increasing CREB1 binding to the COX-2 promoter and the expression of COX-2 in human amnion fibroblasts. This feed-forward loop may be crucial for the production of prostaglandins in the fetal membranes prior to the onset of labor.
Regulation of Estradiol and Progesterone Production by CRH-R1 and -R2 Is through Divergent Signaling Pathways in Cultured Human Placental Trophoblasts
Authors: Gao Lu , Tao Yi , Hu Tianxiao , Liu Weina , Xu Chen , Liu Jie , You Xingji , Gu Hang , Ni Xin 
Published: September 2012

Abstract
CRH and its related peptides urocortins (UCN) have been identified in placenta and implicated to play pivotal roles in the regulation of pregnancy and parturition in humans. The objectives of present study were to investigate the effects of endogenous CRH and its related peptides in the regulation of steroid production in placenta. Placental trophoblasts were isolated from term placenta tissues and cultured for 72 h. Estradiol (E2) and progesterone (P4) contents in culture media were determined by radioimmunoassay. Treatment of cultured trophoblasts with CRH or UCNI antibody showed decreased E2, whereas increased P4 production. Treatment of cells with CRH receptor type 1 antagonist antalarmin or CRH receptor type 2 (CRH-R2) antagonist astressin-2b also decreased E2 but increased P4 production. Knockdown of CRH receptor type 1 or CRH-R2 cells showed a decrease in E2 production and an increase in P4 production. In CRH-R2 knockdown cells, CRH stimulated GTP-bound Gαs protein and phosphorylated phospholipase C-β3. Adenylyl cyclase and protein kinase A inhibitors blocked CRH-induced increased E2 production but not decreased P4 production. PLC inhibitor U73122 and protein kinase C inhibitor chelerythrine blocked the effects of CRH on E2 and P4 production in CRH-R2 knockdown cells. UCNIII, the specific CRH-R2 agonist, stimulated GTP-bound Gαi protein and phosphorylated phospholipase C-β3 expression. Both U73122 and chelerythrine blocked UCNIII-induced increased E2 production and decreased P4 production. We suggest that CRH and its related peptides might be involved in changes in the progesterone to estrogen ratio during human pregnancy.
The Organizational and Aromatization Hypotheses Apply to Rapid, Nonclassical Hormone Action: Neonatal Masculinization Eliminates Rapid Estradiol Action in Female Hippocampal Neurons
Authors: Meitzen John , Grove Danielle D. , Mermelstein Paul G. 
Published: September 2012

Abstract
Early exposure to the steroid sex hormone testosterone and its estrogen metabolite estradiol masculinize neural tissue during a developmental critical period. Many aspects of neuron anatomy and physiology are permanently altered, including later sensitivity to estradiol. Although it is well established that early hormone exposure alters neuronal responsiveness regarding classical estradiol actions (i.e. acting via nuclear estrogen receptors), it has not yet been determined whether it also alters neuronal processing of nonclassical estrogen receptor signaling, including the actions of membrane-associated estrogen receptors. Hence, we tested whether membrane estrogen receptor regulation of cAMP response element binding protein (CREB) phosphorylation observed in female (but not male) hippocampal pyramidal neurons is due to the lack of androgen and/or estrogen exposure in females during this critical period. Female rat neonates on postnatal d 0 and 1 were systemically injected with one of four compounds: vehicle, testosterone, the nonaromatizable androgen dihydrotestosterone, or estradiol. On postnatal d 2, primary hippocampal neuron cultures were generated from these animals. After 8–9 d in culture, we assessed whether estradiol affected CREB phosphorylation. Neurons from female neonates exposed to testosterone lacked estradiol signaling to CREB. In contrast, dihydrotestosterone injections of female neonates did not disrupt estradiol regulation of CREB. Estradiol injections of female neonates, however, eliminated estradiol signaling to CREB. These findings indicate that testosterone aromatization to estradiol leads to a masculinization/defeminization process whereby hippocampal neurons fail to exhibit rapid estradiol signaling to CREB. Broadly, these findings extend the organizational and aromatization hypotheses to rapid, nonclassical hormone action.
Low Degree of Overlap Between Kisspeptin, Neurokinin B, and Dynorphin Immunoreactivities in the Infundibular Nucleus of Young Male Human Subjects Challenges the KNDy Neuron Concept
Authors: Hrabovszky Erik , Sipos Máté T. , Molnár Csilla S. , Ciofi Philippe , Borsay Beáta Á. , Gergely Péter , Herczeg László , Bloom Stephen R. , Ghatei Mohammad A. , Dhillo Waljit S. , Liposits Zsolt 
Published: September 2012

Abstract
Previous immunohistochemical and in situ hybridization studies of sheep, goats, and rodents indicated that kisspeptin (KP), neurokinin B (NKB), and dynorphin A (DYN) are extensively colocalized in the hypothalamic arcuate nucleus, thus providing a basis for the KP/NKB/DYN (KNDy) neuron concept; in both sexes, KNDy neuropeptides have been implicated in the generation of GnRH neurosecretory pulses and in the negative feedback effects of sexual steroids to the reproductive axis. To test the validity and limitations of the KNDy neuron concept in the human, we carried out the comparative immunohistochemical analysis of the three neuropeptides in the infundibular nucleus (Inf; also known as arcuate nucleus) and stalk of young male human individuals (&lt;37 yr). Results of quantitative immunohistochemical experiments established that the regional densities of NKB immunoreactive (IR) perikarya and fibers, and the incidence of afferent contacts they formed onto GnRH neurons, were about 5 times as high as those of the KP-IR elements. Dual-immunofluorescent studies confirmed that considerable subsets of the NKB-IR and KP-IR cell bodies and fibers are separate, and only about 33% of NKB-IR perikarya and 75% of KP-IR perikarya were dual labeled. Furthermore, very few DYN-IR cell bodies could be visualized in the Inf. DYN-IR fibers were also rare and, with few exceptions, distinct from the KP-IR fibers. The abundance and colocalization patterns of the three immunoreactivities showed similar trends in the infundibular stalk around portal blood vessels. Together these results indicate that most NKB neurons in the Inf do not synthesize detectable amounts of KP and DYN in young male human individuals. These data call for a critical use of the KNDy neuron terminology when referring to the putative pulse generator system of the mediobasal hypothalamus. We conclude that the functional importance of these three neuropeptides in reproductive regulation considerably varies among species, between sexes, and at different ages.
Applicability of the doubly labelled water method to the rhinoceros auklet, Cerorhinca monocerata
Authors: Shirai Masaki , Ito Motohiro , Yoda Ken , Niizuma Yasuaki 
Published: September 2012

Summary
The doubly labelled water (DLW) method is an isotope-based technique that is used to measure the metabolic rates of free-living animals. We validated the DLW method for measuring metabolic rates in five rhinoceros auklets (Cerorhinca monocerata) compared with simultaneous measurements using the respirometric method. We calculated the CO2 production rate of four auklets (mean initial body mass: 552 g±36 s.d.) injected with DLW, using the one- and two-pool models. The metabolic rate during the 24-h measurements in a respirometric chamber for resting auklets averaged 16.30±1.66 kJ h−1 (n = 4). The metabolic rates determined using the one- and two-pool models in the DLW method for the same period as the respirometric measurement averaged 16.61±2.13 kJ h−1 (n = 4) and 16.16±2.10 kJ h−1 (n = 4), respectively. The mean absolute percent error between the DLW and respirometric methods was 8.04% using the one-pool model and was slightly better than that with the two-pool model. The differences in value between the DLW and respirometric methods are probably due to oxygen isotope turnover, which eliminated only 10–14% of the initial enrichment excess.
Chicken primordial germ cells use the anterior vitelline veins to enter the embryonic circulation
Authors: De Melo Bernardo Ana , Sprenkels Kaylee , Rodrigues Gabriela , Noce Toshiaki , Chuva De Sousa Lopes Susana M. 
Published: September 2012

Summary
During gastrulation, chicken primordial germ cells (PGCs) are present in an extraembryonic region of the embryo from where they migrate towards the genital ridges. This is also observed in mammals, but in chicken the vehicle used by the migratory PGCs is the vascular system. We have analysed the migratory pathway of chicken PGCs, focusing on the period of transition from the extraembryonic region to the intraembryonic vascular system.
Our findings show that at Hamburger and Hamilton developmental stage HH12–HH14 the majority of PGCs concentrate axially in the sinus terminalis and favour transport axially via the anterior vitelline veins into the embryonic circulation. Moreover, directly blocking the blood flow through the anterior vitelline veins resulted in an accumulation of PGCs in the anterior region and a decreased number of PGCs in the genital ridges. We further confirmed the key role for the anterior vitelline veins in the correct migration of PGCs using an ex ovo culture method that resulted in defective morphogenetic development of the anterior vitelline veins.
We propose a novel model for the migratory pathway of chicken PGCs whereby the anterior vitelline veins play a central role at the extraembryonic and embryonic interface. The chicken model of PGC migration through the vasculature may be a powerful tool to study the process of homing (inflammation and metastasis) due to the striking similarities in regulatory signaling pathways (SDF1–CXCR4) and the transient role of the vasculature.
The interrelationship between APC/C and Plk1 activities in centriole disengagement
Authors: Hatano Toshiyuki , Sluder Greenfield 
Published: September 2012

Summary
Mother–daughter centriole disengagement, the necessary first step in centriole duplication, involves Plk1 activity in early mitosis and separase activity after APC/C activity mediates securin degradation. Plk1 activity is thought to be essential and sufficient for centriole disengagement with separase activity playing a supporting but non-essential role. In separase null cells, however, centriole disengagement is substantially delayed. The ability of APC/C activity alone to mediate centriole disengagement has not been directly tested. We investigate the interrelationship between Plk1 and APC/C activities in disengaging centrioles in S or G2 HeLa and RPE1 cells, cell types that do not reduplicate centrioles when arrested in S phase. Knockdown of the interphase APC/C inhibitor Emi1 leads to centriole disengagement and reduplication of the mother centrioles, though this is slow. Strong inhibition of Plk1 activity, if any, during S does not block centriole disengagement and mother centriole reduplication in Emi1 depleted cells. Centriole disengagement depends on APC/C–Cdh1 activity, not APC/C–Cdc20 activity. Also, Plk1 and APC/C–Cdh1 activities can independently promote centriole disengagement in G2 arrested cells. Thus, Plk1 and APC/C–Cdh1 activities are independent but slow pathways for centriole disengagement. By having two slow mechanisms for disengagement working together, the cell ensures that centrioles will not prematurely separate in late G2 or early mitosis, thereby risking multipolar spindle assembly, but rather disengage in a timely fashion only late in mitosis.
A role for Rap2 in recycling the extended conformation of LFA-1 during T cell migration
Authors: Stanley Paula , Tooze Sharon , Hogg Nancy 
Published: September 2012

Summary
T lymphocytes make use of their major integrin LFA-1 to migrate on surfaces that express ICAM-1 such as blood vessels and inflamed tissue sites. How the adhesions are turned over in order to supply traction for this migration has not been extensively investigated. By following the fate of biotinylated membrane LFA-1 on T lymphocytes, we show in this study that LFA-1 internalization and re-exposure on the plasma membrane are linked to migration. Previously we demonstrated the GTPase Rap2 to be a regulator of LFA-1-mediated migration. SiRNA knockdown of this GTPase inhibits both LFA-1 internalization and also its ability to be re-exposed, indicating that Rap2 participates in recycling of LFA-1 and influences its complete endocytosis–exocytosis cycle. Confocal microscopy images reveal that the intracellular distribution of Rap2 overlaps with endosomal recycling vesicles. Although the homologous GTPase Rap1 is also found on intracellular vesicles and associated with LFA-1 activation, these two homologous GTPases do not co-localize. Little is known about the conformation of the LFA-1 that is recycled. We show that the extended form of LFA-1 is internalized and in Rap2 siRNA-treated T lymphocytes the trafficking of this LFA-1 conformation is disrupted resulting in its intracellular accumulation. Thus LFA-1-mediated migration of T lymphocytes requires Rap2-expressing vesicles to recycle the extended form of LFA-1 that we have previously found to control migration at the leading edge.
Apoptosis ofAscogregarina taiwanensis(Apicomplexa: Lecudinidae) which failed to migrate within its natural host
Authors: Chen Wei-June , Huang Ching-Gi , Fan-Chiang Mei-Huei , Liu Yu-Han , Lee Yi-Feng 
Published: September 2012

SummarySexual reproduction of Ascogregarina taiwanensis (Apicomplexa: Lecudinidae), a parasite specific to the mosquito Aedes albopictus, in malpighian tubules is initiated by the entry of the trophotozoites developed in the midgut shortly afterpupation (usually &lt; 5 h). However, only a low proportion of trophozoites are able to migrate; others end up dying. In this study, we demonstrated those trophozoites which failed to migrate eventually died of apoptosis. Morphological changes such as shrinkage, chromatin aggregations, and formation of blunt ridges on the surface were seen in moribund trophozoites. In addition, DNA fragmentation of trophozoites isolated from the midgut of pupae was demonstrated by the presence of DNA ladders, Annexin V staining, and TUNEL assays. Due to detection of caspase-like activity, apoptosis of those trophozoites may have occurred through a mechanism of an intrinsic or mitochondrial-mediated pathway. Although apoptosis has been observed in various species of protozoa, it is not clear how apoptosis in single-celled organisms might result from evolution by natural selection. However, we speculate that apoptosis may regulate the parasite load of A. taiwanensis within its natural mosquito host, leading to an optimized state of the survival rate for both parasite and host.
Micro-, Meso-, and Macroporous Materials Obtained from a Highly Concentrated Emulsion of Decane/Brij 35/Water and Decane/Brij 700/Water
Authors: Santamaría Esther , Cortés Marta , Maestro Alicia , Porras Montserrat , Gutiérrez Jose Maria , González Carmen 
Published: September 2012

Abstract
Mesoporous materials have high potential for use as catalyst supports. Different formation mechanisms for mesostructured materials have already been described. In the present study, different micro-, meso-, and macroporous materials were obtained from highly concentrated emulsions, and the possibility of raw materials recovery was investigated. The materials, including that synthesized from a recovered surfactant, were tested as Nafion catalyst supports. Moreover, ordered mesoporous materials were obtained through another formation mechanism, namely, cooperative autoassembling, and the influence of the preparation and composition variables on the specific area of the materials was studied.