bluuebunny/crossref_metadata_2025_split huggingface dataset:
Wnt signaling regulates homeostasis of the periodontal ligament
Authors: Lim W. H. , Liu B. , Cheng D. , Williams B. O. , Mah S. J. , Helms J. A. 
Published: January 2014

Background and ObjectiveIn health, the periodontal ligament maintains a constant width throughout an organism's lifetime. The molecular signals responsible for maintaining homeostatic control over the periodontal ligament are unknown. The purpose of this study was to investigate the role of Wnt signaling in this process by removing an essential chaperone protein, Wntless (Wls), from odontoblasts and cementoblasts, and observing the effects of Wnt depletion on cells of the periodontal complex.Material and MethodsThe Wnt responsive status of the periodontal complex was assessed using two strains of Wnt reporter mice: Axin2LacZ/+ and Lgr5LacZ/+. The function of this endogenous Wnt signal was evaluated by conditionally eliminating the Wntless (Wls) gene using an osteocalcin Cre driver. The resulting OCN‐Cre;Wls fl/fl mice were examined using micro‐computed tomography and histology, immunohistochemical analyses for osteopontin, Runx2 and fibromodulin, in‐situ hybridization for osterix and alkaline phosphatase activity.ResultsThe adult periodontal ligament is Wnt responsive. Elimination of Wnt signaling in the periodontal complex of OCN‐Cre;Wlsfl/fl mice resulted in a wider periodontal ligament space. This pathologically increased periodontal width is caused by a reduction in the expression of osteogenic genes and proteins, which results in thinner alveolar bone. A concomitant increase in fibrous tissue occupying the periodontal space was observed, along with a disruption in the orientation of the periodontal ligament.ConclusionThe periodontal ligament is a Wnt‐dependent tissue. Cells in the periodontal complex are Wnt responsive, and eliminating an essential component of the Wnt signaling network leads to a pathological widening of the periodontal ligament space. Osteogenic stimuli are reduced, and a disorganized fibrillary matrix results from the depletion of Wnt signaling. Collectively, these data underscore the importance of Wnt signaling in homeostasis of the periodontal ligament.
Prostaglandin E2 inhibits in‐vitro mineral deposition by human periodontal ligament cells via modulating the expression of TWIST1 and RUNX2
Authors: Manokawinchoke J. , Pimkhaokhum A. , Everts V. , Pavasant P. 
Published: January 2014

Background and ObjectiveProstaglandin E2 (PGE2) has been shown to be able to influence both bone formation and resorption. The purpose of this study was to investigate the effect of PGE2 on the osteogenic differentiation of human periodontal ligament (HPDL) cells.Material and MethodsHPDL cells were cultured with 0.001–1 μm PGE2 in osteogenic medium. In‐vitro mineral deposition was determined by Alizarin Red S staining, and gene expression was determined by real‐time PCR.ResultsPGE2 inhibited in‐vitro mineral deposition by HPDL cells in a dose‐dependent manner. PCR analyses showed that PGE2 upregulated the expression of Runt‐related transcription factor 2 (RUNX2), but had no effect on osteocalcin expression. Upregulation of TWIST‐related protein1 (TWIST1), a functional antagonist of RUNX2, was also observed. In addition, increased levels of RUNX2 and TWIST1 proteins, induced by PGE2, were detected by western blot analysis. Using a chemical activator of E prostanoid (EP) receptors as well as small interfering RNA against an EP receptor, it was shown that PGE2 regulated RUNX2 and TWIST1 via the EP2 receptor. The role of protein kinase A in the inductive effect of PGE2 was also demonstrated.ConclusionThe results of this study revealed that PGE2 modulates the osteogenic differentiation of HPDL cells via regulating the expression of RUNX2 and TWIST1. The results suggest a possible role for PGE2 in regulating the homeostasis of periodontal ligament tissue.
Placenta Growth Factor and Vascular Endothelial Growth Factor A Have Differential, Cell‐Type Specific Patterns of Expression in Vascular Cells
Authors: Xiang Lingjin , Varshney Rohan , Rashdan Nabil A. , Shaw Jennifer H. , Lloyd Pamela G. 
Published: January 2014

AbstractObjectivePLGF, a VEGF‐A related protein, mediates collateral enlargement via monocytes but plays little role in capillary proliferation. In contrast, VEGF‐A mediates both collateral enlargement and capillary proliferation. PLGF has been less thoroughly studied than VEGF‐A, and questions remain regarding its regulation and function. Therefore, our goal was to characterize the expression of PLGF by vascular cells. We hypothesized that vascular SMC would express more PLGF than EC, since VEGF‐A is primarily expressed by non‐EC.MethodsWe compared PLGF and VEGF‐A across eight EC and SMC lines, then knocked down PLGF and evaluated cell function. We also assessed the effect of hypoxia on PLGF expression and promoter activity.ResultsPLGF was most highly expressed in EC, whereas VEGF‐A was most highly expressed in SMC. PLGF knockdown did not affect EC number, migration, or tube formation, but reduced monocyte migration toward EC. Monocyte migration was rescued by exogenous PLGF. Hypoxia increased PLGF protein without activating PLGF gene transcription.ConclusionsPLGF and VEGF‐A have distinct patterns of expression in vascular cells. EC derived PLGF may function primarily in communication between EC and circulating cells. Hypoxia increases EC PLGF expression posttranscriptionally.
Using encapsulated freeze‐dried lipids to trigger a gastrointestinal vagal reflex: validation in a pig model
Authors: Val‐Laillet D. , Guerin S. , Malbert C.‐H. 
Published: January 2014

AbstractBackgroundNutrient‐sensing studies in humans frequently use intragastric intubation. A non‐invasive alternative would be the use of freeze‐dried lipids (FDL) capsules. We proposed to validate this method in pigs by (i) demonstrating that low‐dose FDL can increase vagal activity, gastric compliance (GC), and delay gastric emptying time (GET); (ii) evaluating the release kinetics of encapsulated FDL.MethodsNine conscious pigs fitted with duodenal catheter and gastric cannula were administered FDL (3‐mL freeze‐dried Intralipid®). Vagal tone was estimated via heart rate variability (HRV) measurements, GC was measured via the barostatic method, and GET after a test meal was evaluated via scintigraphy. FDL vs placebo (methylcellulose [MC]) capsules release kinetics were also evaluated via scintigraphy.Key ResultsDuodenal FDL infusion increased GC in 2/8 trials only, but systematically delayed GET compared to saline (96 vs 70 min; p = 0.018). The presence of FDL in the duodenum decreased heart rate, increased vagal tone, and HRV. FDL capsules released their content in the duodenum before MC capsules (41 vs 67 min; p = 0.013), and MC induced ECG data quite similar to FDL except for HRV (p = 0.011).Conclusions & InferencesLow‐dose FDL was a potent signal to induce vagal reflex and increase GET. FDL capsules released their content in the duodenum and activated the vagal pathway after approximately 40 min, which is an important data for designing future paradigms in humans. MC was not a good placebo because of its stickiness and ability to activate the vagal pathway too.
Pain management during bone marrow aspiration and biopsy in pediatric cancer patients
Authors: Kato Yoko , Maeda Miho , Aoki Yuki , Ishii Eizaburo , Ishida Ysushi , Kiyotani Chikako , Goto Shoko , Sakaguchi Sachi , Sugita Kenichi , Tokuyama Mika , Nakadate Hisaya , Kikuchi Akira , Tsuchida Masahiro , Ohara Akira 
Published: January 2014

AbstractBackgroundThe pain associated with bone marrow aspiration and biopsy (BMAB) has an enormous impact on pediatric cancer patients and their families, but no specific reference standards for sedation and analgesia have been developed inJapan. To determine the problems associated with pain management duringBMAB, a cross‐sectional investigation was conducted.MethodsA survey was sent inOctober 2011 to data managers in institutions belonging to theTokyoChildren'sCancerStudyGroup, addressing the non‐pharmacological and pharmacological pain management forBMABperformed on pediatric cancer inpatients betweenJanuary 2010 andDecember 2010.ResultsThe eligible response rate was 41 of 57 institutions (71.9%). Non‐pharmacological pain intervention was provided in 68% of surveyed institutions. All institutions provided pharmacological pain management. In most institutions, sedation/analgesia was performed by pediatric oncologists in a treatment room in the ward. Standards for pain management were developed and utilized in only four institutions. Other means of pain management were provided in various settings. Twelve institutions reported insufficient sedation/analgesia. In total, 80% of institutions reported some adverse events. Two serious adverse events were reported in cases of underlying or complicated conditions. No serious long‐term consequences were reported.ConclusionsSignificant issues were identified regarding the efficacy and safety of pain management. Adverse events can occur in any institution. Children with underlying or complicated conditions are at high risk for serious adverse events. Therefore, adequate and systematic assessment, patient monitoring, preparation and treatment for adverse events, and cooperation with skilled specialists of pediatric oncology, anesthesiology, and intensive care are essential.
CCR7 facilitates the pro‐inflammatory function of dendritic cells in experimental leishmaniasis
Authors: Kling J. C. , Darby J. , Körner H. 
Published: January 2014

SummaryCutaneous leishmaniasis, caused by the parasite Leishmania major, results in lesions at the site of infection, which are self‐healing in resistant hosts. However, in the absence of the chemokine receptor CCR7, mice are unable to heal the lesion and develop chronic disease. These B6.CCR7−/− mice display an increased number of Th2 cells and immunosuppressive cytokine levels, as well as more regulatory T cells. As CCR7 is expressed on activated dendritic cells (DCs), and these cells require CCR7 to migrate to the draining lymph node, we expected decreased migration of DCs into the lymph node in the absence of CCR7 during cutaneous leishmaniasis. Consequently, in an attempt to initiate a self‐healing response, we adoptively transferred CCR7+ (B6.WT) DCs into the site of infection of B6.CCR7−/− mice. Surprisingly, instead of healing the lesion, B6.CCR7−/− mice inoculated with B6.WT DCs developed augmented lesions and showed increased immunosuppression compared to control B6.CCR7−/− mice transferred with B6.CCR7−/− DCs or B6.WT mice with B6.WT DCs. Finally, B6.WT mice injected with B6.CCR7−/− DCs also presented delayed healing of the lesion. These results indicate that CCR7 must be expressed on DCs, as well as peripheral cells, to allow an efficient immune response to L. major.
Cocaine: The Complementarity Between Legal and Illegal Trade
Authors: Russo Francesco Flaviano 
Published: January 2014

AbstractI show that the decreased price of cocaine in its major destination markets is partly explained by a lower smuggling cost, which is itself the consequence of an increased international trade in legal goods. First, because more legal imports are associated with a bigger number of transporters and therefore with a bigger supply of potential drug smugglers. Second, because, as the number of legal shipments grows, the individual inspection probability decreases, lowering the risk born by the smugglers and thus their compensation. The cocaine market provides evidence of a complementarity between legal and illegal trade.
Angiotensin‐converting enzyme (ACE and ACE2) imbalance correlates with the severity of cerulein‐induced acute pancreatitis in mice
Authors: Liu Ruixia , Qi Haiyu , Wang Jing , Wang Yan , Cui Lijian , Wen Yan , Yin Chenghong 
Published: January 2014

New Findings
What is the central question of this study?
Angiotensin‐converting enzyme 2 (ACE2) degrades angiotensin II to angiotensin‐(1–7) and has recently been described to have an antagonistic effect on angiotensin‐converting enzyme (ACE) signalling. However, the specific underlying role of ACE2 in the pathogenesis of severe acute pancreatitis (SAP) is unclear.
What is the main finding and its importance?
Using wild‐type, ACE2 knock‐out and ACE2 transgenic mice, we show that ACE2–ACE imbalance plays an important role in the pathogenesis of SAP and that pancreatic ACE2 is an important factor in determining the severity of SAP.
Angiotensin‐converting enzyme (ACE) and its effector peptide angiotensin II (Ang II) have been implicated in the pathogenesis of pancreatitis. Angiotensin‐converting enzyme 2 (ACE2) degrades Ang II to angiotensin‐(1–7) [Ang‐(1–7)] and has recently been described to have an antagonistic effect on ACE signalling. However, the specific underlying role of ACE2 in the pathogenesis of severe acute pancreatitis (SAP) is unclear. In the present study, the local imbalance of ACE and ACE2, as well as Ang II and Ang‐(1–7) expression, was compared in wild‐type (WT) and ACE2 knock‐out (KO) or ACE2 transgenic (TG) mice subjected to cerulein‐induced SAP. Serum amylase, tumour necrosis factor‐α, interleukin (IL)‐1β, IL‐6 and IL‐10 levels and histological morphometry were used to determine the severity of pancreatitis. In WT mice, pancreatic ACE and Ang II and serum Ang II expression increased (P < 0.05), while pancreatic ACE2 and Ang‐(1–7) and serum Ang‐(1–7) levels were also significantly elevated (P < 0.05) from 2 to 72 h after the onset of SAP. However, the ratio of pancreatic ACE2 to ACE expression was significantly reduced (from 1.46 ± 0.09 to 0.27 ± 0.05, P < 0.001) and paralleled the severity of pancreatitis. The Ace2 KO mice exhibited increased levels of tumour necrosis factor‐α, IL‐1β, IL‐6, multifocal coagulative necrosis and inflammatory infiltrate, and lower levels of serum IL‐10 and pancreatic Ang‐(1–7) (4.70 ± 2.13 versus 10.87 ± 2.51, P < 0.001) compared with cerulein‐treated WT mice at the same time point. Conversely, Ace2 TG mice with normal ACE expression were more resistant to SAP challenge as evidenced by a decreased inflammatory response, attenuated pathological changes and increased survival rates. These data suggest that the ACE2–ACE imbalance plays an important role in the pathogenesis of SAP and that pancreatic ACE2 is an important factor in determining the severity of SAP.
Model Organisms Retain an “Ecological Memory” of Complex Ecologically Relevant Environmental Variation
Authors: Beer Karlyn D. , Wurtmann Elisabeth J. , Pinel Nicolás , Baliga Nitin S. 
Published: January 2014

ABSTRACT

Although tractable model organisms are essential to characterize the molecular mechanisms of evolution and adaptation, the ecological relevance of their behavior is not always clear because certain traits are easily lost during long-term laboratory culturing. Here, we demonstrate that despite their long tenure in the laboratory, model organisms retain “ecological memory” of complex environmental changes. We have discovered that
Halobacterium salinarum
NRC-1, a halophilic archaeon that dominates microbial communities in a dynamically changing hypersaline environment, simultaneously optimizes fitness to total salinity, NaCl concentration, and the [K]/[Mg] ratio. Despite being maintained under controlled conditions over the last 50 years, peaks in the three-dimensional fitness landscape occur in salinity and ionic compositions that are not replicated in laboratory culturing but are routinely observed in the natural hypersaline environment of this organism. Intriguingly, adaptation to variations in ion composition was associated with differential regulation of anaerobic metabolism genes, suggesting an intertwined relationship between responses to oxygen and salinity. Our results suggest that the ecological memory of complex environmental variations is imprinted in the networks for coordinating multiple cellular processes. These coordination networks are also essential for dealing with changes in other physicochemically linked factors present during routine laboratory culturing and, hence, retained in model organisms.
Oxidation of Metabolites Highlights the Microbial Interactions and Role of
Acetobacter pasteurianus
during Cocoa Bean Fermentation
Authors: Moens Frédéric , Lefeber Timothy , De Vuyst Luc 
Published: January 2014

ABSTRACT

Four cocoa-specific acetic acid bacterium (AAB) strains, namely,
Acetobacter pasteurianus
386B,
Acetobacter ghanensis
LMG 23848
T
,
Acetobacter fabarum
LMG 24244
T
, and
Acetobacter senegalensis
108B, were analyzed kinetically and metabolically during monoculture laboratory fermentations. A cocoa pulp simulation medium (CPSM) for AAB, containing ethanol, lactic acid, and mannitol, was used. All AAB strains differed in their ethanol and lactic acid oxidation kinetics, whereby only
A. pasteurianus
386B performed a fast oxidation of ethanol and lactic acid into acetic acid and acetoin, respectively. Only
A. pasteurianus
386B and
A. ghanensis
LMG 23848
T
oxidized mannitol into fructose. Coculture fermentations with
A. pasteurianus
386B or
A. ghanensis
LMG 23848
T
and
Lactobacillus fermentum
222 in CPSM for lactic acid bacteria (LAB) containing glucose, fructose, and citric acid revealed oxidation of lactic acid produced by the LAB strain into acetic acid and acetoin that was faster in the case of
A. pasteurianus
386B. A triculture fermentation with
Saccharomyces cerevisiae
H5S5K23,
L. fermentum
222, and
A. pasteurianus
386B, using CPSM for LAB, showed oxidation of ethanol and lactic acid produced by the yeast and LAB strain, respectively, into acetic acid and acetoin. Hence, acetic acid and acetoin are the major end metabolites of cocoa bean fermentation. All data highlight that
A. pasteurianus
386B displayed beneficial functional roles to be used as a starter culture, namely, a fast oxidation of ethanol and lactic acid, and that these metabolites play a key role as substrates for
A. pasteurianus
in its indispensable cross-feeding interactions with yeast and LAB during cocoa bean fermentation.
Biogeography of the Sediment Bacterial Community Responds to a Nitrogen Pollution Gradient in the East China Sea
Authors: Xiong Jinbo , Ye Xiansen , Wang Kai , Chen Heping , Hu Changju , Zhu Jianlin , Zhang Demin 
Published: January 2014

ABSTRACT

Patterns of microbial distribution represent the integrated effects of historical and biological processes and are thus a central issue in ecology. However, there is still active debate on whether dispersal limitation contributes to microbial diversification in strongly connected systems. In this study, sediment samples were collected along a transect representing a variety of seawater pollution levels in the East China Sea. We investigated whether changes in sediment bacterial community structures would indicate the effects of the pollution gradient and of dispersal limitation. Our results showed consistent shifts in bacterial communities in response to pollution. More geographically distant sites had more dissimilar communities (
r
= −0.886,
P
< 0.001) in this strongly connected sediment ecosystem. A variance analysis based on partitioning by principal coordinates of neighbor matrices (PCNM) showed that spatial distance (dispersal limitation) contributed more to bacterial community variation (8.2%) than any other factor, although the environmental factors explained more variance when combined (11.2%). In addition, potential indicator taxa (primarily affiliated with
Deltaproteobacteria
and
Gammaproteobacteria
) were identified; these taxa characterized the pollution gradient. This study provides direct evidence that dispersal limitation exists in a strongly connected marine sediment ecosystem and that candidate indicator taxa can be applied to evaluate coastal pollution levels.
Prevalence in Bulk Tank Milk and Epidemiology of
Campylobacter jejuni
in Dairy Herds in Northern Italy
Authors: Bianchini Valentina , Borella Laura , Benedetti Valentina , Parisi Antonio , Miccolupo Angela , Santoro Eliana , Recordati Camilla , Luini Mario 
Published: January 2014

ABSTRACT

Thermotolerant
Campylobacter
spp. are frequently the cause of human gastroenteritis and have assumed more importance in Italy following the increased consumption of raw milk. Our objectives were to determine the prevalence and genotypes of
Campylobacter
spp. in dairy herds and to investigate the possible sources of bulk milk contamination. Bulk milk from dairy herds (
n
= 282) was cultured for
Campylobacter
spp. and
Enterobacteriaceae
. At three
Campylobacter jejuni
-positive farms, bovine feces, pigeon intestines, milk, and water points were also investigated. Isolates were identified by PCR and genotyped using multilocus sequence typing (MLST).
C. jejuni
was detected in 34 (12%) bulk milk samples. The strains belonged to 14 sequence types, and the most common clonal complexes were CC-21, CC-48, and CC-403. No association was demonstrated between the presence of
C. jejuni
and high levels of
Enterobacteriaceae
in bulk milk. At the three farms examined,
C. jejuni
was isolated from bovine feces (25/82 [30.5%]), pigeon intestines (13/60 [21.7%]), bulk milk (10/24 [41.7%]), and water points (4/16 [25%]). MLST revealed lineages that were common between milk and bovine feces but distinct between cattle and pigeons. In one herd,
C. jejuni
with the same genotype was isolated repeatedly from bulk milk and a cow with an udder infection. Our results showed a high prevalence of
C. jejuni
in bulk milk and suggested that udder excretion, in addition to fecal matter, may be a route of bulk milk contamination. MLST analysis indicated that pigeons are probably not relevant for the transmission of
C. jejuni
to cattle and for milk contamination.
Synergistic Bactericidal Effect of Simultaneous Near-Infrared Radiant Heating and UV Radiation against
Cronobacter sakazakii
in Powdered Infant Formula
Authors: Ha Jae-Won , Kang Dong-Hyun 
Published: January 2014

ABSTRACT

The aim of this study was to investigate the synergistic bactericidal effects of the simultaneous application of near-infrared (NIR) heating and UV irradiation against
Cronobacter sakazakii
in powdered infant formula and to determine the effect on quality by measuring color changes and performing sensory evaluation. A cocktail of
C. sakazakii
strains was inoculated into powdered infant formula, followed by NIR, UV, and combined NIR-UV treatments. The sum of NIR and UV inactivation was lower than that obtained by the simultaneous application of both technologies due to their synergism. Simultaneous NIR-UV combined treatment for 7 min achieved a 2.79-log-unit CFU reduction of
C. sakazakii
. The underlying inactivation mechanisms of the combined NIR-UV treatment were evaluated by the propidium iodide (PI) uptake test, and we confirmed that disruption of the bacterial cell membrane was the main factor contributing to the synergistic lethal effect. The color values and sensory characteristics of simultaneously NIR-UV-treated infant formula powder were not significantly (
P
> 0.05) different from those of the control. The results of this study suggest that a NIR-UV decontaminating system can be applied as an alternative to other interventions in powdered weaning foods.