bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Ramadan fasting in Saudi Arabia on serum bone profile and immunoglobulins
Authors: Bahijri Suhard M. , Ajabnoor Ghada M. , Borai Anwar , Al-Aama Jumana Y. , Chrousos George P. 
Published: July 2015

Background: Each year Muslims fast from dawn to sunset for 1 month (Ramadan). In Saudi Arabia, the sleep–wake cycle during Ramadan is severely disturbed and is associated with abolition of the circadian cortisol rhythm, exposing Saudis to continuously increased cortisol levels, which may influence the immune response. In addition to cortisol, sleep and fasting affect the secretion of parathyroid hormone (PTH) and hence bone metabolism. Methods: Our objective was to investigate the effect of Ramadan type fasting on secretory patterns of PTH, markers of bone metabolism, and serum immunoglobulins. Blood samples from healthy young volunteers were collected at 9 a.m. and 9 p.m. (± 1 hour) before (Shaban) and 2 weeks into Ramadan. Calcium, phosphorus, magnesium, albumin, alkaline phosphatase, 25-OH vitamin D, intact PTH (iPTH), and immunoglobulin (Ig) A, M and G were measured. Results: During Ramadan, evening-adjusted calcium was higher ( p = 0.036) and phosphate lower ( p < 0.001) than the corresponding morning value. Moreover, the Ramadan mean morning phosphate was higher and the evening level lower was than Shabaan values ( p = 0.010 and p <0.001, respectively), while mean iPTH level was decreased compared with the morning value ( p = 0.001), and the evening mean during Shabaan ( p = 0.029). Mean IgG concentration was significantly lower during Ramadan ( p = 0.003 and p = 0.021 for morning and evening, respectively). Conclusions: Changes in dietary practices during Ramadan modulated PTH secretion to a pattern which might be beneficial to bone health. Combined effects of fasting and disturbed sleep led to a noted decrease in IgG level. Therefore, a possible beneficial effect of fasting on bone turnover is combined with decreased immune response.
Novel whole blood assay for phenotyping platelet reactivity in mice identifies ICAM-1 as a mediator of platelet-monocyte interaction
Authors: Armstrong Paul C. J , Kirkby Nicholas S. , Chan Melissa V. , Finsterbusch Michaela , Hogg Nancy , Nourshargh Sussan , Warner Timothy D. 
Published: July 2015

Key PointsLow-volume, high-throughput whole blood aggregometry will facilitate future mouse platelet function research. Application of this approach identifies ICAM-1 as a novel mediator of platelet-monocyte interaction through fibrinogen binding.
RETRACTED ARTICLE: Mechanistic attributes of S100A7 (psoriasin) in resistance of anoikis resulting tumor progression in squamous cell carcinoma of the oral cavity
Authors: Dey Kaushik Kumar , Sarkar Siddik , Pal Ipsita , Das Subhasis , Dey Goutam , Bharti Rashmi , Banik Payel , Roy Joygopal , Maity Sukumar , kulavi Indranil , Mandal Mahitosh 
Published: July 2015

Abstract
Background
Squamous cell carcinoma of the oral cavity (SCCOC) is the dominant origin of cancer associated mortality. Previous findings by our study reported that acquisition of anoikis resistance has a significant role in tumor progression of oral cavity. Several genes were over-expressed in anoikis-resistant cells under detached conditions which we confirmed earlier by microarray. Normal oral squamous epithelia grow adherent to a basement membrane, and when detached from the extracellular matrix, undergoes programmed cell death. The acquisition of anoikis-resistance is crucial phenomena in oral tumor advancement. In the current study, we have identified S100A7 expression as contributing factor for anoikis resistance and tumorigenicity in human oral cancer cells. Further, we have explored that elevated S100A7 expression in anoikis-sensitive oral keratinocytes and cancer cells reshape them more resistant to anoikis and apoptosis inducers via activation of cellular intrinsic and extrinsic avenue.

Methods
A subset of human cancer cell lines TU167, JMAR, JMARC39, JMARC42 and MDA-MB-468 were utilized for the generation of resistant stable cell lines. Further, immunohistochemistry, western blot and immunoprecipitation, assays of apoptosis, soft agar assay, orthotopic animal model and signaling elucidation were performed to establish our hypothesis.

Results
S100A7 gene is found to be responsible for anoikis resistance and tumorigenicity in human oral cancer cells. We have observed up-regulation of S100A7 in anoikis resistant cell lines, orthotropic model and patients samples with head and neck cancer. It is also noticed that secretion of S100A7 protein in conditioned medium by anoikis resistant head & neck cancer cell and in saliva of head and neck cancer patients. Up-regulation of S100A7 expression has triggered enhanced tumorigenicity and anchorage-independent growth of cancer cells through Akt phosphorylation leading to development of aniokis resistance in head and neck cancer cells.

Conclusions
These data have led us to conclude that S100A7 is the major contributing factor in mediating anoikis-resistance of oral cancer cells and local tumor progression, and S100A7 might be useful as diagnostic marker for early detection of primary and recurrent squamous cell cancer.
Next-generation sequencing to guide cancer therapy
Authors: Gagan Jeffrey , Van Allen Eliezer M. 
Published: July 2015

AbstractAs a result of multiple technological and practical advances, high-throughput sequencing, known more commonly as “next-generation” sequencing (NGS), can now be incorporated into standard clinical practice. Whereas early protocols relied on samples that were harvested outside of typical clinical pathology workflows, standard formalin-fixed, paraffin-embedded specimens can more regularly be used as starting materials for NGS. Furthermore, protocols for the analysis and interpretation of NGS data, as well as knowledge bases, are being amassed, allowing clinicians to act more easily on genomic information at the point of care for patients. In parallel, new therapies that target somatically mutated genes identified through clinical NGS are gaining US Food and Drug Administration (FDA) approval, and novel clinical trial designs are emerging in which genetic identifiers are given equal weight to histology. For clinical oncology providers, understanding the potential and the limitations of DNA sequencing will be crucial for providing genomically driven care in this era of precision medicine.
Global genetic carrier testing: a vision for the future
Authors: Beaudet Arthur L. 
Published: July 2015

Editorial summaryExpanded genetic carrier testing is changing clinical practice. Current experience highlights the need for rigorous curation of tens of thousands of variants as to their pathogenicity and phenotypic effects. There is an urgent need for strategies to present a range of options to families to enable them to make informed decisions. The potential exists to avoid the great majority of serious inherited, but not de novo, single-gene disabilities.
Hypoxia accelerates vascular repair of endothelial colony-forming cells on ischemic injury via STAT3-BCL3 axis
Authors: Lee Sang Hun , Lee Jun Hee , Han Yong-Seok , Ryu Jung Min , Yoon Yeo Min , Han Ho Jae 
Published: July 2015

Abstract
Introduction
Endothelial colony-forming cells (ECFCs) significantly improve tissue repair by providing regeneration potential within injured cardiovascular tissue. However, ECFC transplantation into ischemic tissue exhibits limited therapeutic efficacy due to poor engraftment in vivo. We established an adequate ex vivo expansion protocol and identified novel modulators that enhance functional bioactivities of ECFCs.

Methods
To augment the regenerative potential of ECFCs, functional bioactivities of hypoxia-preconditioned ECFCs (hypo-ECFCs) were examined.

Results
Phosphorylations of the JAK2/STAT3 pathway and clonogenic proliferation were enhanced by short-term ECFC culturing under hypoxia, whereas siRNA-targeting of STAT3 significantly reduced these activities. Expression of BCL3, a target molecule of STAT3, was increased in hypo-ECFCs. Moreover, siRNA inhibition of BCL3 markedly reduced survival of ECFCs during hypoxic stress in vitro and ischemic stress in vivo. In a hindlimb ischemia model of ischemia, hypo-ECFC transplantation enhanced blood flow ratio, capillary density, transplanted cell proliferation and survival, and angiogenic cytokine secretion at ischemic sites.

Conclusions
Hypoxia preconditioning facilitates functional bioactivities of ECFCs by mediating regulation of the STAT3-BCL3 axis. Thus, a hypoxic preconditioned ex vivo expansion protocol triggers expansion and functional bioactivities of ECFCs via modulation of the hypoxia-induced STAT3-BCL3 axis, suggesting that hypo-ECFCs offer a therapeutic strategy for accelerated neovasculogenesis in ischemic diseases.
Determination of hydrogen cyanide concentration in mainstream smoke of tobacco products by polarography
Authors: Mahernia Shabnam , Amanlou Arash , kiaee Gita , Amanlou Massoud 
Published: July 2015

Abstract

Background
There has been a worldwide concern for the health risks of cigarette smoking and hydrogen cyanide (HCN) considered as one of the hazardous tobacco compounds which is needed to be determined in order to reduce the dose related to smoke disease risk.
In this study, we prepare the experimental procedure to entrap the HCN from mainstream smoke of different brands of Tehran cigarette, through simulating human inhalation and determine its concentration applying polarography.

Results
The HCN level of the 50 commonly consumed tobacco products (47 cigarettes and 3 cigars) obtained from local store is ranged between 17.56 ± 1.02 and 1553.98 ± 0.56 μg per stick, this acquired amount is more than FDA approval (10 μg per stick), so the harmful effects of smoking is indicative.

Conclusions
The comparative study of the results shows that the price and the weight of each product do not indicate HCN level. As can be seen, R2 value which is a statistical measure of how close the data are to the fitted regression line is low (R2 < 0.2). So it should not be deceived by names such as ultra light or infinite gravity to suck, because this names or the price haven’t effect on the amount of HCN and its destructive effects.
The sulfidation process of sterling silver in different corrosive environments: impact of the process on the surface films formed and consequences for the conservation-restoration community
Authors: Storme Patrick , Schalm Olivier , Wiesinger Rita 
Published: July 2015

Abstract

Background
Precious objects made of silver and/or its alloys tarnish and become black when exposed to ambient atmospheres containing moisture and ppb-amounts of H2S. Such objects usually contain small but variable amounts of copper as alloying constituent and this affects the corrosion process due to a preferential oxidation of copper. However the visual appearance of the formed tarnishing layers on different types of silver alloys is very similar. Therefore, conservators-restorers are confronted with the problem that in some cases certain cleaning techniques are very effective while in other similar cases the removal of tarnishing layers is unsatisfactory. Since cleaning experiments are not allowed on genuine objects, many investigations use artificially corroded dummies instead. In order to evaluate the representativity and reproducibility of this often used methodology, differences in morphology, microstructure and composition of the sulfide layers on sterling silver generated by different sulfidation methods were analysed.

Results
Sterling silver samples were artificially aged in five different environments. The samples exposed to uncontrolled ambient air at different locations (e.g. residential and laboratory environments) showed different corrosion rates and corrosion colours. Three accelerated ageing methods were executed in a gaseous or liquid environment under controlled conditions. These tests showed different results in morphology, microstructure, composition, thickness and the interface between bulk and corrosion layer. A first accelerated sulfidation procedure in a Na2S solution alternated with exposure to air, resulted in a fast corrosion rate and an even corrosion layer formation with several S-species. A second series of sulfidation in a controlled gas environment of H2S and SO2 developed a thin but uneven corrosion layer, mainly consisting of oxides. A third corrosion methodology used was based on the thioacetamide method. This resulted in an even and relative thick corrosion layer, comparable to the Na2S/aeration sulfidation system. However, the interface between the corrosion layer and the bulk is importantly different, showing severe voids.

Conclusions
The corrosion layers generated by five different experimental sulfidation series on identical prepared sterling silver coupons were clearly different from each other. Analyses demonstrated that the composition and microstructure of the corrosion layers were strongly dependent on the sulfidation method used and copper was found to be an important element present in all sulfide layers analysed. Therefore, artificially corroded sterling silver is not necessarily representative for naturally tarnished historical objects and the extrapolation of the cleaning results obtained on dummies to historical objects must be performed with care.
Stock assessment and management implications of an endemic fish, Oxygymnocypris stewartii, in the Yarlung Zangbo River in Tibet, China
Authors: Huo Bin , Ma Bao Shan , Xie Cong Xin , Duan You Jian , Yang Xue Feng , Huang Hai Ping 
Published: July 2015

AbstractBackgroundOxygymnocypris stewartiiis an endemic species only inhabiting the middle and upper reaches of the Yarlung Zangbo River and its tributaries at altitudes above 3600 m in the Qinghai-Tibet Plateau and has suffered a continuous decline of population size owing to anthropogenic disturbance. However, little is known about the stock status of this species and how to protect it. In this study, we evaluated the population status ofO. stewartiiand investigated two management policies including the minimum age limits and seasonal closure in the Yarlung Zangbo River.ResultsEstimates of the total mortality rate were 0.35 year−1for females and 0.65 year−1for males. The natural mortality rates were estimated as 0.10 and 0.22 year−1for females and 0.12 and 0.29 year−1for males using two empirical methods. TheO. stewartiipopulation may be in near full exploitation under the current harvesting strategy in the Yarlung Zangbo River, with a high chance of recruitment failure in the future. Although both minimum age limits and seasonal closure could be effective measures to conserve theO. stewartiistock, it was proposed that a seasonal closure was implemented each year from September to December according to the complexity of the application and the effects on the income of local fishermen and on the biological invasion.ConclusionsThe stock ofO. stewartiimay be in near full exploitation under the current harvesting strategy, with a high chance of recruitment failure in the future. Our results indicated that the imposition of the seasonal closure from September to December might be the effective measure to conserve theO. stewartiipopulation.
The evaluation of a scoring system in airway management after oral cancer surgery
Authors: Lee Ho-Jin , Kim Jin-Wook , Choi So-Young , Kim Chin-Soo , Kwon Tae-Geon , Paeng Jun-Youg 
Published: July 2015

Abstract

Background
The purpose of this retrospective study was to investigate the usefulness of tracheostomy scoring system in the decision of postoperative airway management in oral cancer patients.

Materials and methods
A total of 104 patients were reviewed in this retrospective study, who underwent radical resection with or without neck dissection and free flap reconstruction due to oral cancer. The patients were classified into three groups according to the timing of the extubation; extubated groups (n = 51), overnight intubation group (n = 45), and tracheostomy group (n = 8). Cameron’s score was used to evaluate the relation between the state of the patient’s airway and the type of the operation.

Results
Tracheostomy was performed in eight patients (8/104, 7.7 %). A total of 22 patients (21.2 %) had more than 5 points of which 17 patients (77.3 %) did not have a tracheostomy and any postoperative emergency airway problems. The tracheostomy scores were significantly different among the three groups. Hospital stay showed a significant correlation with the tracheostomy score.

Conclusions
The scoring system did not quite agree with the airway management of the authors’ clinic; however, it can be one of the clinical factors predicting the degree of the postoperative airway obstruction and surgical aggressiveness for recovery. The further studies are needed for clinically more reliable scoring systems.
Neutrophils rapidly transit inflamed lymphatic vessel endothelium via integrin-dependent proteolysis and lipoxin-induced junctional retraction
Authors: Rigby David A , Ferguson David J P , Johnson Louise A , Jackson David G 
Published: July 2015

AbstractNeutrophils are the first leukocyte population to be recruited from the circulation following tissue injury or infection, where they play key roles in host defense. However, recent evidence indicates recruited neutrophils can also enter lymph and shape adaptive immune responses downstream in draining lymph nodes. At present, the cellular mechanisms regulating neutrophil entry to lymphatic vessels and migration to lymph nodes are largely unknown. Here, we have investigated these events in an in vivo mouse Mycobacteriumbovis bacillus Calmette-Guérin vaccination model, ex vivo mouse dermal explants, and in vitro Transwell system comprising monolayers of primary human dermal lymphatic endothelial cells. We demonstrate that neutrophils are reliant on endothelial activation for adhesion, initially via E-selectin and subsequently, by integrin-mediated binding to ICAM-1 and VCAM-1, combined with CXCL8-dependent chemotaxis. Moreover, we reveal that integrin-mediated neutrophil adhesion plays a pivotal role in subsequent transmigration by focusing the action of matrix metalloproteinases and the 15-lipoxygenase-1-derived chemorepellent 12(S)-hydroxyeicosatetraenoic acid at neutrophil:endothelial contact sites to induce transient endothelial junctional retraction and rapid, selective neutrophil trafficking. These findings reveal an unexpectedly intimate collaboration between neutrophils and the lymphatic vessel endothelium, in which these phagocytic leukocytes act as pathfinders for their own transit during inflammation.
Intravenous immunoglobulin skews macrophages to an anti-inflammatory, IL-10-producing activation state
Authors: Kozicky Lisa K , Zhao Zheng Yu , Menzies Susan C , Fidanza Mario , Reid Gregor S D , Wilhelmsen Kevin , Hellman Judith , Hotte Naomi , Madsen Karen L , Sly Laura M 
Published: July 2015

Abstract
Intravenous Ig is used to treat autoimmune or autoinflammatory disorders, but the mechanism by which it exerts its immunosuppressive activity is not understood completely. To examine the impact of intravenous Ig on macrophages, we compared cytokine production by LPS-activated macrophages in the presence and absence of intravenous Ig. Intravenous Ig treatment induced robust production of IL-10 in response to LPS, relative to LPS stimulation alone, and reduced production of proinflammatory cytokines. This anti-inflammatory, intravenous Ig-induced activation was sustained for 24 h but could only be induced if intravenous Ig were provided within 1 h of LPS stimulation. Intravenous Ig activation led to enhanced and prolonged activation of MAPKs, Erk1/2, p38, and Erk5, and inhibition of each reduced intravenous Ig-induced IL-10 production and suppression of IL-12/23p40. IL-10 production occurred rapidly in response to intravenous Ig + LPS and was sufficient to reduce proinflammatory IL-12/23p40 production in response to LPS. IL-10 induction and reduced IL-12/23p40 production were transcriptionally regulated. IL-10 played a direct role in reducing proinflammatory cytokine production by macrophages treated with intravenous Ig + LPS, as macrophages from mice deficient in the IL-10R β chain or in IL-10 were compromised in their ability to reduce proinflammatory cytokine production. Finally, intraperitoneal injection of intravenous Ig or intravenous Ig + LPS into mice activated macrophages to produce high levels of IL-10 during subsequent or concurrent LPS challenge, respectively. These findings identify IL-10 as a key anti-inflammatory mediator produced by intravenous Ig-treated macrophages and provide insight into a novel mechanism by which intravenous Ig may dampen down inflammatory responses in patients with autoimmune or autoinflammatory diseases.
Rapid externalization of 27-kDa heat shock protein (HSP27) and atypical cell death in neutrophils treated with the sphingolipid analog drug FTY720
Authors: Skrzeczyńska-Moncznik Joanna , Bzowska Małgorzata , Nogieć Anna , Sroka Agnieszka , Zarebski Mirosław , Vallières Luc , Guzik Krzysztof 
Published: July 2015

Abstract
The sphingolipid analog fingolimod is known to induce apoptosis of tumor cells and lymphocytes. Its effect on neutrophils has not been investigated so far. Here, we describe a fingolimod-induced atypical cell death mechanism in human neutrophils, characterized by rapid translocation of heat shock protein 27 to the cell surface, extensive cell swelling and vacuolization, atypical chromatin staining and nuclear morphology, and phosphorylation of mixed lineage kinase domain-like protein. Fingolimod also induces typical apoptotic features, including rapid externalization of phosphatidylserine and activation of caspase-8. Fingolimod-induced neutrophil death is independent of sphingosine-1-phosphate receptors and positively regulated by protein phosphatase A. Externalization of phosphatidylserine and heat shock protein 27 can be partially inhibited by inhibitors of caspase-8 [Z-Ile-Glu(O-Me)-Thr-Asp(O-Me)-fluoromethyl ketone], receptor-interacting protein kinase 1 (necrostatin-1), receptor-interacting protein kinase 3 (necrosulfonamide), and heat shock protein 90 [geldanamycin and 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin]. Furthermore, NADPH oxidase 1 inhibition with diphenyleneiodonium chloride protects neutrophils against fingolimod-mediated cell death. Overall, these observations suggest that fingolimod acts through a mechanism involving the necrosome signaling complex and the oxidative stress machinery.