bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of dietary deviation on disease progression and gut microbiome composition in lupus-prone SNF1 mice
Authors: Johnson B M , Gaudreau M-C , Al-Gadban M M , Gudi R , Vasu C 
Published: February 2015

Summary
Environmental factors, including microbes and diet, play a key role in initiating autoimmunity in genetically predisposed individuals. However, the influence of gut microflora in the initiation and progression of systemic lupus erythematosus (SLE) is not well understood. In this study, we have examined the impact of drinking water pH on immune response, disease incidence and gut microbiome in a spontaneous mouse model of SLE. Our results show that (SWR × NZB) F1 (SNF1) mice that were given acidic pH water (AW) developed nephritis at a slower pace compared to those on neutral pH water (NW). Immunological analyses revealed that the NW-recipient mice carry relatively higher levels of circulating autoantibodies against nuclear antigen (nAg) as well as plasma cells. Importantly, 16S rRNA gene-targeted sequencing revealed that the composition of gut microbiome is significantly different between NW and AW groups of mice. In addition, analysis of cytokine and transcription factor expression revealed that immune response in the gut mucosa of NW recipient mice is dominated by T helper type 17 (Th17) and Th9-associated factors. Segmented filamentous bacteria (SFB) promote a Th17 response and autoimmunity in mouse models of arthritis and multiple sclerosis. Interestingly, however, not only was SFB colonization unaffected by the pH of drinking water, but also SFB failed to cause a profound increase in Th17 response and had no significant effect on lupus incidence. Overall, these observations show that simple dietary deviations such as the pH of drinking water can influence lupus incidence and affect the composition of gut microbiome.
Evaluation of the first maxillary molar post‐extraction socket as a model for dental implant osseointegration research
Authors: Du Zhibin , Lee Ryan S. B. , Hamlet Stephen , Doan Nghiem , Ivanovski Saso , Xiao Yin 
Published: February 2015

AbstractObjectivesPublished information regarding the use of rat jawbones for dental implant osseointegration research is limited and often inconsistent. This study assessed the suitability and feasibility of placing dental implants into the rat maxilla and to establish parameters to be used for dental implant research using this model.Materials and methodsForty‐two customized titanium implants (2 × 3 mm) were placed bilaterally in the maxillary first molar area of 21 Sprague–Dawley rats. Every animal received two implants. The animals were subsequently sacrificed at days 3, 7, 14, 28 and 56 post‐surgery. Resin‐embedded sections of the implant and surrounding maxilla were prepared for histological and histomorphometric analyses.ResultsThe mesial root of the first molar in the rat maxilla was the optimal site to place the implant. Although the most apical 2–3 threads of the implant penetrated into the sinus cavity, 2 mm of the remaining implant was embedded in the bone. New bone formation at day 7 around the implant increased further at day 14, as measured by the percentage of bone‐to‐implant contact (%BIC) and new bone area (%BA) in the implant thread chambers (55.1 ± 8.9% and 63.7 ± 7.7%, respectively). There was a further significant increase between day 14 and 28 (P < 0.05), however, no significant differences were found between day 28 and 56 in either %BIC or %BA.ConclusionsThe mesial root socket of the first molar in the rat maxilla is a useful model for dental implant research. Osseointegration following implant placement as measured by BIC plateaued after 28 days. The recommended implant dimensions are 1.5 mm in diameter and 2 mm in length.
Hypomagnesaemia and its potential impact on thiamine utilisation in patients with alcohol misuse at the Alice Springs Hospital
Authors: Dingwall Kylie Maree , Delima Jennifer Flavia , Gent Debra , Batey Robert Gordon 
Published: February 2015

AbstractIntroduction and AimsAlcohol rapidly reduces thiamine among alcohol‐dependent individuals. Poor diet and alcohol's impact on absorption, storage, activation and excretion of thiamine are thought to be the mechanisms. Previous literature identifies magnesium as an important cofactor in thiamine utilisation, which might also be compromised in alcohol dependent patients. The aim was to describe the thiamine status and clinical profile for a sample of heavy alcohol users entering the Alice Springs Hospital in the Northern Territory of Australia and to examine the relationship between thiamine deficiency, magnesium deficiency and cognitive functioning.Design and MethodsCross‐sectional study examining thiamine pyrophosphate (TPP) and magnesium concentrations for a sample of 62 males and 43 females (N = 105; n = 88 Aboriginal, n = 13 non‐Indigenous). Cognition was assessed using the Rowland Universal Dementia Assessment Scale.ResultsTPP concentrations were within or above the reference range. Aboriginal patients had significantly lower TPP than non‐Indigenous patients. A marginally significant difference was found between individuals with thiamine supplementation recorded within the previous 20 days compared with those without. Mean serum magnesium was in the low normal range with magnesium deficiency (i.e. <0.80 mmol L−1) present in 48% of those tested. Serum magnesium (but not TPP) concentrations correlated positively with cognitive test scores.Discussion and ConclusionsDespite increased exposure to risk factors for Wernicke Korsakoff Syndrome, no patient had TPP concentrations below the reference range. High patient readmission and aggressive thiamine treatment policies may explain this finding. However, low magnesium may be prevalent and could contribute to impaired thiamine utilisation. [Dingwall KM, Delima JF, Gent D, Batey RG. Hypomagnesaemia and its potential impact on thiamine utilisation in patients with alcohol misuse at the Alice Springs Hospital. Drug Alcohol Rev 2015]
Effects of lowering the alcohol minimum purchasing age on weekend hospitalised assaults of young Māori in New Zealand
Authors: Kypri Kypros , Davie Gabrielle , McElduff Patrick , Langley John , Connor Jennie 
Published: February 2015

AbstractIntroduction and AimsWe examine the association between reducing the alcohol minimum purchasing age from 20 to 18 years in December 1999 and rates of weekend assault hospitalisation among young Māori in the following 12 years. Our previous work showed deleterious effects for young people overall. In keeping with Treaty of Waitangi principles, we sought to determine whether the policy was similarly detrimental for Māori.Design and MethodsWe used Poisson regression to examine data from 1995 to 2011 on Māori hospitalised on Friday–Sunday following assault, separately by gender among 15‐ to 17‐year‐olds and 18‐ to 19‐year‐olds, versus 20‐ to 21‐year‐olds as a control for changes in economic and environmental factors.ResultsThere was no evidence to suggest weekend assault hospitalisations increased significantly more among 15‐ to 17‐year‐old or 18‐ to 19‐year‐old Māori males in the post‐change periods (incidence rate ratios varied between 0.83 and 1.13; P values >0.25) compared with increases observed in 20‐ to 21‐year‐old Māori males. For Māori females, estimates were more variable, but overall, there was no evidence of the hypothesised effect (incidence rate ratios between 0.60 and 1.09; P values >0.07).Discussion and ConclusionsOverall, we find no evidence that lowering the minimum alcohol purchasing age increased weekend hospitalised assaults among young Māori. Inferences are compromised by lack of statistical power which underlines the importance of planning for evaluation of important policies well before they are implemented, particularly with a view to meeting obligations to Māori arising from the Treaty of Waitangi. [Kypri K, Davie G, McElduff P, Langley J, Connor J. Effects of lowering the alcohol minimum purchasing age on weekend hospitalised assaults of young Māori in New Zealand. Drug Alcohol Rev 2015]
Periostin, a neurite outgrowth‐promoting factor, is expressed at high levels in the primate cerebral cortex
Authors: Matsunaga Eiji , Nambu Sanae , Oka Mariko , Tanaka Michio , Taoka Miki , Iriki Atsushi 
Published: February 2015

Periostin (POSTN or osteoblast specific factor) is an extracellular matrix protein originally identified as a protein highly expressed in osteoblasts. Recently, periostin has been reported to function in axon regeneration and neuroprotection. In the present study, we focused on periostin function in cortical evolution. We performed a comparative gene expression analysis of periostin between rodents (mice) and primates (marmosets and macaques). Periostin was expressed at higher levels in the primate cerebral cortex compared to the mouse cerebral cortex. Furthermore, we performed overexpression experiments of periostin in vivo and in vitro. Periostin exhibited neurite outgrowth activity in cortical neurons. These results suggested the possibility that prolonged and increased periostin expression in the primate cerebral cortex enhances the cortical plasticity of the mammalian cerebral cortex.
Effects of sitagliptin on counter‐regulatory and incretin hormones during acute hypoglycaemia in patients with type 1 diabetes: a randomized double‐blind placebo‐controlled crossover study
Authors: Schopman J. E. , Hoekstra J. B. L. , Frier B. M. , Ackermans M. T. , de Sonnaville J. J. J. , Stades A. M. , Zwertbroek R. , Hartmann B. , Holst J. J. , Knop F. K. , Holleman F. 
Published: February 2015

AimsTo assess whether the dipeptidyl peptidase‐4 (DPP‐4) inhibitor sitagliptin affects glucagon and other counter‐regulatory hormone responses to hypoglycaemia in patients with type 1 diabetes.MethodsWe conducted a single‐centre, randomized, double‐blind, placebo‐controlled, three‐period crossover study. We studied 16 male patients with type 1 diabetes aged 18–52 years, with a diabetes duration of 5–20 years and intact hypoglycaemia awareness. Participants received sitagliptin (100 mg/day) or placebo for 6 weeks and attended the hospital for three acute hypoglycaemia studies (at baseline, after sitagliptin treatment and after placebo). The primary outcome was differences between the three hypoglycaemia study days with respect to plasma glucagon responses from the initialization phase of the hypoglycaemia intervention to 40 min after onset of the autonomic reaction.ResultsSitagliptin treatment significantly increased active levels of glucose‐dependent insulinotropic polypeptide and glucagon‐like peptide‐1. No significant differences were observed for glucagon or adrenergic counter‐regulatory responses during the three hypoglycaemia studies. Growth hormone concentration at 40 min after occurrence of autonomic reaction was significantly lower after sitagliptin treatment [median (IQR) 23 (0.2–211.0) mEq/l] compared with placebo [median (IQR) 90 (8.8–180) mEq/l; p = 0.008].ConclusionsSitagliptin does not affect glucagon or adrenergic counter‐regulatory responses in patients with type 1 diabetes, but attenuates the growth hormone response during late hypoglycaemia.
Using multiple traits to estimate the effects of heat shock on the fitness of Aphidius colemani
Authors: Jerbi‐Elayed Mey , Lebdi‐Grissa Kaouthar , Foray Vincent , Muratori Frédéric , Hance Thierry 
Published: February 2015

AbstractExtreme temperature events are a great challenge for most ectotherms, particularly for the immature stages of parasitoids, as they do not possess the ability to behaviourally thermoregulate. In this study, we measured the effect of an acute heat shock, combined with desiccation stress (34 °C and 35% r.h. during 10 h) during the mummy stage on several fitness‐related traits of emerging adults of the aphid parasitoid Aphidius colemani Viereck (Hymenoptera: Braconidae: Aphidiinae). Our results showed that the emergence rate was strongly affected by the heat shock (63 ± 2.3 vs. 96.1 ± 0.7% for stress vs. control conditions, respectively), and the resulting population was male biased. Heat stress reduced the lifespan of emerged parasitoids but had no effect on fat reserves and female size. Egg load at emergence and parasitism rate were also reduced by heat treatment. The antennal symmetry was disturbed by the heat treatment, and stressed individuals had reduced mating success compared to control parasitoids. Specifically, time before wing fanning, a typical male courtship behaviour, was significantly longer in parasitoid pairs involving females that had emerged from heat‐treated mummies. Additionally, olfactometry tests on experimental females indicated that their response to host odour was similar to that of control individuals, but they required a longer time for perception. These results highlight that exposure to high temperatures during the mummy stage has cumulative detrimental effects that may strongly impact parasitoid populations under natural conditions and hinder the success of biological control programs.
A prospective analysis of clinical efficacy and safety in chronic myeloid leukemia‐chronic phase patients with imatinib resistance or intolerance as evaluated using European LeukemiaNet 2013 criteria
Authors: Murai Kazunori , Akagi Tomoaki , Shimosegawa Kenji , Sugawara Tomohiro , Ishizawa Kenichi , Ito Shigeki , Murai Keiko , Motegi Mutsuhito , Yokoyama Hisayuki , Noji Hideyoshi , Tajima Katsushi , Kimura Jun , Chou Takaaki , Ogawa Kazuei , Harigae Hideo , Kubo Kohmei , Oba Koji , Sakamoto Junichi , Ishida Yoji 
Published: February 2015

AbstractBackgroundWe conducted a phase II study to evaluate the efficacy and safety of dasatinib in Japanese patients with imatinib‐resistant or imatinib‐intolerant chronic myeloid leukemia (CML).MethodsFrom 2009 to 2011, 54 CML‐chronic phase (CP) patients with resistance (n = 40) or intolerance (n = 25) to imatinib were registered to undergo dasatinib treatment. Eleven patients showed both resistance and intolerance to imatinib. Coincidentally, the resistance criteria in this study were the same as a non‐optimal response to tyrosine kinase inhibitors (TKIs) as defined in the European LeukemiaNet (ELN) 2013 recommendations.ResultsThe overall incidence rate of major molecular response (MMR) at 12 months was 62.3% (n = 47). Forty patients with resistance to imatinib who were ‘warning’ and ‘failure’ patients based on the ELN 2013 recommendations were assessed; cumulative MMR and MR4.5 rates were 62.5% (n = 39) and 21.0% (n = 40), respectively, at 12 months. Twelve patients who showed a BCR‐ABL transcript level >1% on the international scale did not achieve a MMR or discontinued dasatinib treatment because of insufficient effects. With regard to safety issues, grade 3/4 non‐hematologic adverse events (AEs) were infrequent.ConclusionsPatients with non‐optimal responses (who meet ELN 2013 warning and failure criteria) to imatinib should be switched quickly to dasatinib, which is less toxic in CML‐CP patients, to improve their prognoses. A BCR‐ABL1 IS of <1% at 3 months of dasatinib administration is a landmark for good therapeutic outcome.
Adenosine A2b receptors control A1 receptor‐mediated inhibition of synaptic transmission in the mouse hippocampus
Authors: Gonçalves Francisco Q. , Pires Johny , Pliassova Anna , Beleza Rui , Lemos Cristina , Marques Joana M. , Rodrigues Ricardo J. , Canas Paula M. , Köfalvi Attila , Cunha Rodrigo A. , Rial Daniel 
Published: February 2015

AbstractAdenosine is a neuromodulator mostly acting through A1 (inhibitory) and A2A (excitatory) receptors in the brain. A2B receptors (A2BR) are Gs/q‐protein‐coupled receptors with low expression in the brain. As A2BR function is largely unknown, we have now explored their role in the mouse hippocampus. We performed electrophysiological extracellular recordings in mouse hippocampal slices, and immunological analysis of nerve terminals and glutamate release in hippocampal slices and synaptosomes. Additionally, A2BR‐knockout (A2BR‐KO) and C57/BL6 mice were submitted to a behavioural test battery (open field, elevated plus‐maze, Y‐maze). The A2BR agonist BAY60‐6583 (300 nm) decreased the paired‐pulse stimulation ratio, an effect prevented by the A2BR antagonist MRS 1754 (200 nM) and abrogated in A2BR‐KO mice. Accordingly, A2BR immunoreactivity was present in 73 ± 5% of glutamatergic nerve terminals, i.e. those immunopositive for vesicular glutamate transporters. Furthermore, BAY 60‐6583 attenuated the A1R control of synaptic transmission, both the A1R inhibition caused by 2‐chloroadenosine (0.1–1 μm) and the disinhibition caused by the A1R antagonist DPCPX (100 nm), both effects prevented by MRS 1754 and abrogated in A2BR‐KO mice. BAY 60‐6583 decreased glutamate release in slices and also attenuated the A1R inhibition (CPA 100 nm). A2BR‐KO mice displayed a modified exploratory behaviour with an increased time in the central areas of the open field, elevated plus‐maze and the Y‐maze and no alteration of locomotion, anxiety or working memory. We conclude that A2BR are present in hippocampal glutamatergic terminals where they counteract the predominant A1R‐mediated inhibition of synaptic transmission, impacting on exploratory behaviour.
Hydroxylated histidine of human ribosomal protein uL2 is involved in maintaining the local structure of 28S rRNA in the ribosomal peptidyl transferase center
Authors: Yanshina Darya D. , Bulygin Konstantin N. , Malygin Alexey A. , Karpova Galina G. 
Published: February 2015

Protein uL2 is essential for the catalytic activity of the ribosome and has a conserved shape in ribosomes from all domains of life. However, the sequence of its unstructured C‐terminal loop apex that contacts the conserved 23S/28S rRNA helix (H) 93 near the ribosomal peptidyl transferase center differs in bacteria, archaea and eukaryotes. Eukaryote‐specific residue His216 located in this loop in mammalian uL2 is hydroxylated in ribosomes. We used a set of chemical probes to explore the structure of an RNA that mimicked a segment of 28S rRNA domain V containing part of the uL2 binding site including H93, complexed with either natural (hydroxylated) or recombinant (unmodified) human uL2. It was found that both protein forms engage H93 during binding, but only natural uL2 (uL2n) protects it from hydroxyl radicals. The association of uL2n with RNA leads to changes in its structure at U4532 adjacent to the universally conserved U4531 (U2585, Escherichia coli numbering) involved in peptidyl transferase center formation, and at the universally conserved C4447 (2501) located in the ribosome near A4397 (2451) and C3909 (2063) belonging to the peptidyl transferase center. As a result, both nucleotides become strongly exposed to hydroxyl radicals. Our data argue that the hydroxyl group at His216 in the C‐terminal loop apex of mammalian uL2 contributes to stabilization of a protein conformation that is favorable for binding to H93 of 28S rRNA and that this binding induces structural rearrangement in the regions close to the peptidyl transferase center in the mature ribosome.
Predicting early life connectivity of Antarctic silverfish, an important forage species along the Antarctic Peninsula
Authors: La Mesa Mario , Piñones Andrea , Catalano Barbara , Ashford Julian 
Published: February 2015

AbstractThe early life stages of the Antarctic silverfish (Pleuragramma antarctica), an important prey species for higher predators in the Southern Ocean ecosystem, dominate the larval fish assemblages of the Bransfield Strait, one of the most important areas for larval retention off the Antarctic Peninsula. Nevertheless, the spatial location of areas where they were spawned and the timing of larval hatching remain unknown. By linking Lagrangian particle tracking simulations with age data obtained using otolith microincrements from fish caught north of Joinville Island in a pelagic survey, we estimated the distribution of hatch dates and subsequent growth rates of silverfish reaching the Bransfield Strait, and predicted the areas where they were spawned. Larval hatching peaked during the last week of December, and the inner shelf and shelf break, east of the Larsen Ice shelf, were the dominant areas predicted to contribute to larval assemblages in the Bransfield Strait. Over simulated periods of 600–630 days, 35–40% of particles remained within the Bransfield Strait, suggesting an important source of supply to higher predators feeding off the northern Antarctic Peninsula. The daily growth rate at the mean size of 22.3 mm was 0.18 mm, corresponding to a daily change in size of approximately 0.82% standard length (SL), and large variability in growth rate suggested a wide range of environmental conditions experienced during the period of advection from the spawning areas. These results provide spatial predictions that can be tested empirically in future studies, using the simulated trajectories to inform sampling design and spatial coverage.
Methyl‐donor deficiency in adolescence affects memory and epigenetic status in the mouse hippocampus
Authors: Tomizawa H. , Matsuzawa D. , Ishii D. , Matsuda S. , Kawai K. , Mashimo Y. , Sutoh C. , Shimizu E. 
Published: February 2015

AbstractDNA methylation is one of the essential factors in the control of gene expression. Alteration of the DNA methylation pattern has been linked to various neurological, behavioral and neurocognitive dysfunctions. Recent studies have pointed out the importance of epigenetics in brain development and functions including learning and memory. Nutrients related to one‐carbon metabolism are known to play important roles in the maintenance of genomic DNA methylation. Previous studies have shown that the long‐term administration of a diet lacking essential one‐carbon nutrients such as methionine, choline and folic acid (methyl donors) caused global DNA hypermethylation in the brain. Therefore, the long‐term feeding of a methyl‐donor‐deficient diet may cause abnormal brain development including learning and memory. To confirm this hypothesis, 3‐week‐old mice were maintained on a folate‐, methionine‐ and choline‐deficient (FMCD) or control (CON) diet for 3 weeks. We found that the methyl‐donor deficiency impaired both novel object recognition and fear extinction after 3 weeks of treatment. The FMCD group showed spontaneous recovery of fear that differed from that in CON. In addition, we found decreased Gria1 gene expression and specific CpG hypermethylation of the Gria1 promoter region in the FMCD hippocampus. Our data suggest that a chronic dietary lack of methyl donors in the developmental period affects learning, memory and gene expressions in the hippocampus.