bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of clinical and radiographic peri‐implant parameters among obese and non‐obese patients: A 5‐year study
Authors: Alkhudhairy Fahad , Vohra Fahim , Al‐Kheraif Abdulaziz A. , Akram Zohaib 
Published: July 2018

AbstractBackgroundIt is postulated that peri‐implant parameters are worse in obese individuals as compared to nonobese.ObjectiveThe aim of the present 5‐year longitudinal study was to analyze and compare the changes in clinical and radiographic peri‐implant parameters among obese and non‐obese patients.Materials and methodsTwenty patients with body mass index ≥ 27.5 kg/m2 and 18 non‐obese controls were included. All patients were indicated for single tooth maxillary or mandibular molar replacement with the adjacent teeth intact. Peri‐implant clinical (plaque index [PI], bleeding on probing [BOP], probing depth [PD]) and radiographic (marginal bone loss [MBL]) parameters were measured at 12, 24, and 60 months of follow‐up.ResultsAll peri‐implant parameters showed statistically significant difference between obese and non‐obese individuals. Obese group recorded significant higher BOP, PD, and MBL at different observation times. Probing depth and MBL increased significantly with advance of time in both groups. After 60 months of follow‐up period, greater PI and BOP was observed in obese patients (P < 0.01). At 60 months follow‐up period, obese patients showed significant increased PD (3.69 mm) as compared to non‐obese individuals (2.46 mm). Marginal bone loss in non‐obese individuals varied from 0.30 mm after 12 months, reaching 0.55 mm after 60 months of follow‐up period, while in obese patients MBL values went from 0.36 mm after 12 months to 0.91 mm at 60 months follow‐up (P < 0.01).ConclusionsPatients with obesity are at risk of increased localized peri‐implant soft and hard tissue inflammation. It is recommended that clinicians should educate obese patients about risk of increased peri‐implant tissue inflammation and susceptibility to bone loss and stipulate stringent oral hygiene care for ideal peri‐implant health.
Prevention and treatment of parastomal hernia: a position statement on behalf of the Association of Coloproctology of Great Britain and Ireland
Authors:   ACPGBI Parastomal Hernia Group
Published: July 2018

AbstractAimThe Association of Coloproctology of Great Britain and Ireland (ACPGBI) Delphi process identified prevention and treatment of parastomal hernia (PSH) as the second highest priority non‐cancer related colorectal pathology. This position statement aims to summarize the current evidence base.MethodsFour broad themes were identified (prevention, diagnosis/classification, management and operative repair). Guidelines are based on evidence from an extensive literature review using organized searches on the PubMed, MEDLINE, Embase and Cochrane databases. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) system was adhered to for classifying the quality of evidence and reporting the strength of recommendations.ResultsThe suture repair of PSH other than for patients in extremis is not recommended. Synthetic non‐absorbable mesh can be used safely in the short term in the construction of colostomies post rectal surgery, but longer‐term follow‐up is needed. Other broad recommendations are made around access to stoma care nurses, prevention classification and management.ConclusionThere is a lack of high quality evidence for many domains in the prevention and treatment of PSH but the results of several studies are awaited.What does this paper add to the literature?Parastomal hernias are a common and debilitating condition following stoma formation. This position statement from ACPGBI details the current evidence base and ongoing research for the prevention, diagnosis and management of parastomal hernias.
The importance of early life experience and animal cultures in reintroductions
Authors: Teitelbaum Claire S. , Converse Sarah J. , Mueller Thomas 
Published: July 2018

AbstractEven within a single population, individuals can display striking differences in behavior, with consequences for their survival and fitness. In reintroduced populations, managers often attempt to promote adaptive behaviors by controlling the early life experiences of individuals, but it remains largely unknown whether this early life training has lasting effects on behavior. We investigated the behavior of reintroduced whooping cranes (Grus americana) trained to migrate using two different methods to see whether their migration behavior remained different or converged over time. We found that the behavior of the two groups converged relatively rapidly, indicating that early life training may not produce lasting effects, especially in species that display lifelong learning and behavioral adaptation. In some cases, managers may consider continual behavioral interventions after release if desired behaviors are not present. Understanding the roles early life experience and animal cultures play in determining behavior is crucial for successful reintroduction programs.
Contactin‐associated protein‐like 2, a protein of the neurexin family involved in several human diseases
Authors: Saint‐Martin Margaux , Joubert Bastien , Pellier‐Monnin Véronique , Pascual Olivier , Noraz Nelly , Honnorat Jérôme 
Published: July 2018

AbstractContactin‐associated protein‐like 2 (CASPR2) is a cell adhesion protein of the neurexin family. Proteins of this family have been shown to play a role in the development of the nervous system, in synaptic functions, and in neurological diseases. Over recent years, CASPR2 function has gained an increasing interest as demonstrated by the growing number of publications. Here, we gather published data to comprehensively review CASPR2 functions within the nervous system in relation to CASPR2‐related diseases in humans. On the one hand, studies on Cntnap2 (coding for CASPR2) knockout mice revealed its role during development, especially, in setting‐up the inhibitory network. Consistent with this result, mutations in the CNTNAP2 gene coding for CASPR2 in human have been identified in neurodevelopmental disorders such as autism, intellectual disability, and epilepsy. On the other hand, CASPR2 was shown to play a role beyond development, in the localization of voltage‐gated potassium channel (VGKC) complex that is composed of TAG‐1, Kv1.1, and Kv1.2. This complex was found in several subcellular compartments essential for action potential propagation: the node of Ranvier, the axon initial segment, and the synapse. In line with a role of CASPR2 in the mature nervous system, neurological autoimmune diseases have been described in patients without neurodevelopmental disorders but with antibodies directed against CASPR2. These autoimmune diseases were of two types: central with memory disorders and temporal lobe seizures, or peripheral with muscular hyperactivity. Overall, we review the up‐to‐date knowledge on CASPR2 function and pinpoint confused or lacking information that will need further investigation.
A dipeptidyl peptidase‐4 inhibitor promotes wound healing in normoglycemic mice by modulating keratinocyte activity
Authors: Shih Chun‐Ming , Huang Chun‐Yao , Huang Chien‐Yu , Wang Kuo‐Hsien , Wei Po‐Li , Chang Yu‐Jia , Fong Tsorng‐Harn , Pan Jun‐Liang , Lee Ai‐Wei 
Published: July 2018

AbstractDipeptidyl peptidase‐4 (DPP‐4) inhibitors are a well‐known and novel class of oral antihyperglycaemic drugs. DPP‐4 inhibition facilitates ulcer healing in patients with diabetes. However, the actual mechanisms, which are independent of lower blood glucose levels, are still unknown. Therefore, the aim of this study was to analyse the effect of the DPP‐4 inhibitor sitagliptin on wound healing through a glucose‐independent pathway. In this study, DPP‐4 inhibitors facilitate keratinocyte differentiation and the proliferation, increase blood flow in the cutaneous of wounds in healthy C57BL/6 mice. Additionally, the administration of the DPP‐4 inhibitor ameliorates wound healing and enhances adiponectin expression in healthy C57BL/6 mice. Taken together, our results reveal a protective role for the DPP‐4 inhibitor sitagliptin in wound healing by regulating adiponectin and phospho‐eNOS levels in keratinocytes. Based on these results, the DPP‐4 inhibitor may have therapeutic potential for healing wounds through a diabetes‐independent mechanism.
Relationships between ecological niche and expected shifts in elevation and latitude due to climate change in South American temperate forest plants
Authors: Alarcón Diego , Cavieres Lohengrin A. 
Published: July 2018

AbstractAimNiche properties, such as breadth and position along environmental gradients, are hypothesized to determine plant responses to climate change. We explored the properties of different plant niches in a biodiversity hotspot, over a wide span of elevational and latitudinal ranges, to assess the relationship between niche characteristics and the modelled distributional shifts due to climate change.LocationSouth American temperate forests.MethodsWe assessed the niche breadth and position of 118 plant species of South American temperate forests, using an Outlying Mean Index (OMI). Bioclimatic information was gathered for each species from WorldClim, and both present and future distributions were modelled using BIOMOD, considering migration constraints with MIGCLIM. The relationships between niche properties and shifts in elevational and latitudinal distributions were explored using linear regressions.ResultsNiche differences among species were related to two bioclimatic dimensions: the first one correlated with the mean diurnal temperature range and precipitation seasonality following the mediterranean—temperate—sub‐Antarctic climatic gradient; the second one correlated with minimum winter temperature along a gradient from oceanic‐influenced habitats to cold tree line habitats. The projected elevational shifts were inversely related to niche breadth and the forecast latitudinal shifts were directly related to niche breadth. The shifts in elevation and latitude for understorey plants were not consistent with the shifts of dominant trees.Main conclusionsThe plant niches were successfully discerned by OMI analyses and they were associated with specific morphological or physiological traits. South American temperate forest plants showed an inverse relationship between niche breadth and elevational shifts, but a positive relationship regarding expected latitudinal shifts. This may be related to the fact that niche drivers followed a latitudinal orientation and the species showed the Rapoport's effect. Thus, the niche breadth and latitudinal position of the species should be considered in climatic change studies.
Time trends regarding the etiology of renal artery stenosis: 18 years’ experience from the China Center for Cardiovascular Disease
Authors: Xiong Hong‐liang , Peng Meng , Jiang Xiong‐jing , Che Wu‐qiang , Dong Hui , Chen Yang , Zou Yu‐bao , Gao Run‐lin , Liu Li-sheng 
Published: July 2018

The time trends regarding the etiology of renal artery stenosis (RAS) are changing, but few investigations have focused on these issues. This study aimed to analyze the time trends regarding the etiology of RAS in a large patient sample from the China Center for Cardiovascular Disease. Consecutive inpatients with RAS from January 1999 to December 2016 were enrolled in this study. The etiologic diagnosis of RAS was based on established criteria. We retrospectively analyzed the time trends regarding the etiology of RAS during an 18‐year period. A total of 2905 patients with RAS were enrolled. There were 2393 (82.4%) patients with atherosclerosis (AS), 345 (11.9%) with Takayasu arteritis (TA), 126 (4.3%) with fibromuscular dysplasia (FMD), and 41 (1.4%) with other causes. Among all patients (n = 2905), patients aged ≤ 40 years (n = 450), patients aged >40 years (n = 2455), female patients (n = 1097), male patients (n = 1808), female patients aged >40 years (n = 808), and male patients aged >40 years (n = 1647), there were a gradual increase in the proportion of atherosclerotic RAS (P < 0.05), a gradual decrease in the proportion of RAS caused by TA (P < 0.05), and almost no change in the proportion of RAS caused by FMD during the 18‐year period (P > 0.05). The data show that the primary causes of RAS are AS, TA, and FMD. The proportion of RAS caused by AS and TA gradually increased and decreased, respectively, over time, and the proportion of RAS caused by FMD showed no significant change.
Tracking pressure injuries as adverse events: National use of the Global Trigger Tool over a 4‐year period
Authors: Gunningberg Lena , Sving Eva , Hommel Ami , Ålenius Carina , Wiger Per , Bååth Carina 
Published: July 2018

AbstractAimTo examine the frequency, preventability, and consequences of hospital acquired pressure injuries in acute care hospitals over a 4‐year period.MethodA retrospective record review was performed using the Swedish version of the Global Trigger Tool (GTT). A total of 64 917 hospital admissions were reviewed. Data were collected between 2013 and 2016 from all 63 Swedish acute care hospitals.ResultsThe prevalence of pressure injuries (category 2‐4) was 1%. Older patients, “satellite patients”, and patients with acute admissions had more pressure injuries. Most pressure injuries (91%) were determined to be preventable. The mean extended length of hospital stay was 15.8 days for patients who developed pressure injuries during hospitalization.ConclusionThe GTT provides a useful and complementary national perspective on hospital acquired pressure injuries across hospitals, informing health care providers on safety priorities to reduce patient harm. Clinical leaders can use information on the preventability and the consequences of pressure injuries, as well as evidence‐based arguments for improving the health care organization.
The mGluR5 positive allosteric modulator VU0409551 improves synaptic plasticity and memory of a mouse model of Huntington's disease
Authors: Doria Juliana G. , de Souza Jessica M. , Silva Flavia R. , Olmo Isabella G. , Carvalho Toniana G. , Alves‐Silva Juliana , Ferreira‐Vieira Talita H. , Santos Jessica T. , Xavier Claudymara Q. S. , Silva Nathalia C. , Maciel Esther M. A. , Conn Peter Jeffrey , Ribeiro Fabiola M. 
Published: July 2018

AbstractHuntington's Disease (HD) is an autosomal‐dominant neurodegenerative disorder, characterized by involuntary body movements, cognitive impairment, and psychiatric disorder. The metabotropic glutamate receptor 5 (mGluR5) plays an important role in HD and we have recently demonstrated that mGluR5‐positive allosteric modulators (PAMs) can ameliorate pathology and the phenotypic signs of a mouse model of HD. In this study, we investigated the molecular mechanisms involved in mGluR5 PAMs effect on memory. Our results demonstrate that subchronic treatment with the mGluR5 PAM VU0409551 was effective in reversing the memory deficits exhibited by BACHD mice, a mouse model for HD. Moreover, VU0409551 treatment stabilized mGluR5 at the cellular plasma membrane of BACHD mice, increasing the expression of several genes important for synaptic plasticity, including c‐Fos, brain‐derived neurotrophic factor, Arc/Arg3.1, syntaxin 1A, and post‐synaptic density‐95. In addition, VU0409551 treatment also increased dendritic spine density and maturation and augmented the number of pre‐synaptic sites. In conclusion, our results demonstrate that VU0409551 triggered the activation of cell signaling pathways important for synaptic plasticity, enhancing the level of dendritic spine maturation and rescuing BACHD memory impairment.Open PracticesOpen Science: This manuscript was awarded with the Open Materials Badge.For more information see: https://cos.io/our-services/open-science-badges/
image
Novel insights into the spatial and temporal complexity of hypothalamic organization through precision methods allowing nanoscale resolution
Authors: Alpár A. , Harkany T. 
Published: July 2018

AbstractThe mammalian hypothalamus contains an astounding heterogeneity of neurons to achieve its role in coordinating central responses to virtually any environmental stressor over the life‐span of an individual. Therefore, while core features of intrahypothalamic neuronal modalities and wiring patterns are stable during vertebrate evolution, integration of the hypothalamus into hierarchical brain‐wide networks evolved to coordinate its output with emotionality, cognition and conscious decision‐making. The advent of single‐cell technologies represents a recent milestone in the study of hypothalamic organization by allowing the dissection of cellular heterogeneity and establishing causality between opto‐ and chemogenetic activity modulation of molecularly‐resolved neuronal contingents and specific behaviours. Thus, organizational rules to accumulate an unprecedented variety of hierarchical neuroendocrine command networks into a minimal brain volume are being unravelled. Here, we review recent understanding at nanoscale resolution on how neuronal heterogeneity in the mammalian hypothalamus underpins the diversification of hormonal and synaptic output and keeps those sufficiently labile for continuous adaptation to meet environmental demands. Particular emphasis is directed towards the dissection of neuronal circuitry for aggression and food intake. Mechanistic data encompass cell identities, synaptic connectivity within and outside the hypothalamus to link vegetative and conscious levels of innate behaviours, and context‐ and circadian rhythm‐dependent rules of synaptic neurophysiology to distinguish hypothalamic foci that either tune the body's metabolic set‐point or specify behaviours. Consequently, novel insights emerge to explain the evolutionary advantages of non‐laminar organization for neuroendocrine circuits coincidently using fast neurotransmitters and neuropeptides. These are then accrued into novel therapeutic principles that meet therapeutic criteria for human metabolic diseases.
Anti‐ApoA‐I IgG antibodies are not associated with carotid artery disease progression and first‐time cardiovascular events in middle‐aged individuals
Authors: Lagerstedt J. O. , Dalla‐Riva J. , Marinkovic G. , Del Giudice R. , Engelbertsen D. , Burlin J. , Petrlova J. , Lindahl M. , Bernfur K. , Melander O. , Nilsson J. , Schiopu A. 
Published: July 2018

AbstractObjectiveIgG antibodies against apolipoprotein A‐I (ApoA‐I) have been found to be elevated in subjects from the general population with clinically manifest cardiovascular disease and in myocardial infarction patients with an adverse prognosis. Here, we investigated whether these antibodies are prospectively associated with carotid artery disease progression and with the risk for first‐time cardiovascular events in individuals with no previous history of cardiovascular disease.Approach and resultsWe selected 383 subjects from the cardiovascular cohort of Malmö Diet and Cancer study who suffered a coronary event during a median follow‐up period of 15.4 (10.3–16.4) years and 395 age‐ and sex‐matched controls. None of the study participants had a previous history of coronary artery disease or stroke. Anti‐ApoA‐I IgG were measured by ELISA in serum samples collected at baseline. Intima‐media thickness (IMT) was measured in the common carotid artery and in the carotid bifurcation at baseline and after 15.9 (±1.5) years. We found no associations between anti‐ApoA‐I IgG and carotid artery IMT at baseline or with IMT progression during follow‐up. In Cox proportional hazards analyses adjusted for traditional cardiovascular risk factors, the hazard ratio (HR 95%CI) for the primary outcome, incident coronary events, was 0.97 (0.75–1.25), P = 0.782, in subjects with anti‐ApoA‐I IgG within the highest tertile compared with the lowest tertile. Similarly, we did not find any associations with the secondary outcome, incident first‐time stroke.ConclusionsSerum autoantibodies against ApoA‐I do not correlate with disease progression and adverse events in cardiovascular disease‐free individuals from the general population.
Fronto‐Insular Connectivity during Pain Distraction Is Impaired in Patients with Somatoform Pain
Authors: Stankewitz Anne , Sorg Christian , von Kalckreuth Alexander , Schulz Enrico , Valet Michael , Neufang Susanne , Zimmer Claus , Henningsen Peter , Gündel Harald , Wohlschläger Afra M. , Tölle Thomas R. 
Published: July 2018

ABSTRACTBACKGROUND AND PURPOSESomatoform pain disorder is characterized by chronic pain and various psychological symptoms including increased attention to mental and physical processes. Given that the medial prefrontal cortex (mPFC) of the default mode network (DMN) and the anterior insula of the salience network are critically involved in intrinsic and attentional processes, we investigated the involvement of these networks during the distraction from physical pain in somatoform pain patients.METHODSDuring painful and nonpainful heat stimulation, attentional distraction from physical processes was modulated with a Stroop task. Thirteen patients were investigated with functional magnetic resonance imaging (fMRI) and compared to 13 controls. Main outcomes were spatial maps of coherent fMRI activity based on independent component analysis and functional connectivity (FC) resulting from psychophysiological interaction analysis.RESULTSBehavioral pain intensity ratings were reduced during the distraction task in both groups. At brain level, we found deviant network activities in the DMN (particularly in the mPFC) and in the salience network (bilaterally in the anterior insula) in patients. During pain stimulation, Stroop‐induced distraction decreased the FC between the mPFC and anterior insula in controls but not in patients.CONCLUSIONSModulating the FC between the mPFC and the insula may be highly relevant for shifting the attention away from external stimuli, including nociceptive input. The observed alterations in somatoform pain patients may foster new strategies in cognitive behavioral training tools for these patients.
Immunoexpression of calcitonin and glucocorticoid receptors in central giant cell lesions of the jaws
Authors: Batista Severo Mara Luana , Lopes Maria Luiza Diniz de Sousa , Miguel Márcia Cristina da Costa , Germano Adriano Rocha , Nogueira Renato Luiz Maia , Turatti Eveline , Cavalcante Roberta Barroso , da Silveira Éricka Janine Dantas 
Published: July 2018

BackgroundThis study analyzed the immunoexpression of calcitonin receptor (CTR) and glucocorticoid receptor (GR) in central giant cell lesions (CGCLs) and verified potential associations with patient's response to clinical treatment with intralesional injection of triamcinolone.Materials and methodsFifty‐four cases of CGCLs, including 22 non‐aggressive, and 32 aggressive, were investigated by immunohistochemistry.ResultsSurgery was the therapeutic choice for 53.1% of the aggressive CGCLs, and 46.9% were submitted to the conservative treatment with intralesional triamcinolone injections. Among patients submitted to conservative treatment, 60% (n = 9) showed favorable response. CTR expression was observed in 68.51%, and GR in 94.44% of the total sample. There were no differences in the expression of CTR, neither GR in mononucleated stromal cells (MSCs) or multinucleated giant cells (MGCs), in relation to aggressiveness, treatment performed for and the response to conservative treatment. Both markers showed a positive correlation between their expression in MSCs and MGCs in the total sample (P < 0.0001). CTR expression on MSCs showed a positive correlation with MGCs in the aggressive and non‐aggressive groups (P < 0.0001).ConclusionsCalcitonin receptor and GR expression were diffuse and similar in non‐aggressive and aggressive cases, and it did not influence the response to clinical treatment with triamcinolone in the sample studied.