bluuebunny/crossref_metadata_2025_split huggingface dataset:
Treatment of aggressive periodontitis
Authors: Teughels Wim , Dhondt Rutger , Dekeyser Christel , Quirynen Marc 
Published: April 2014

AbstractDespite etiological differences between aggressive and chronic periodontitis, the treatment concept for aggressive periodontitis is largely similar to that for chronic periodontitis. The goal of treatment is to create a clinical condition that is conducive to retaining as many teeth as possible for as long as possible. When a diagnosis has been made and risk factors have been identified, active treatment is commenced. The initial phase of active treatment consists of mechanical debridement, either alone or supplemented with antimicrobial drugs. Scaling and root planing has been shown to be effective in improving clinical indices, but does not always guarantee long‐term stability. Antimicrobials can play a significant role in controlling aggressive periodontitis. Few studies have been published on this subject for localized aggressive periodontitis, but generalized aggressive periodontitis has been subject to more scrutiny. Studies have demonstrated that systemic antibiotics as an adjuvant to scaling and root planing are more effective in controlling disease compared with scaling and root planing alone or with supplemental application of local antibiotics or antiseptics. It has also become apparent that antibiotics ought to be administered with, or just after, mechanical debridement. Several studies have shown that regimens of amoxicillin combined with metronidazole or regimens of clindamycin are the most effective and are preferable to regimens containing doxycycline. Azithromycin has been shown to be a valid alternative to the regimen of amoxicillin plus metronidazole. A limited number of studies have been published on surgical treatment in patients with aggressive periodontitis, but the studies available show that the effect can be comparable with the effect on patients with chronic periodontitis, provided that proper oral hygiene is maintained, a strict maintenance program is followed and modifiable risk factors are controlled. Both access surgery and regenerative techniques have shown good results in patients with aggressive periodontitis. Once good periodontal health has been obtained, patients must be enrolled in a strict maintenance program that is directed toward controlling risk factors for disease recurrence and tooth loss. The most significant risk factors are noncompliance with regular maintenance care, smoking, high gingival bleeding index and poor plaque control. There is no evidence to suggest that daily use of antiseptic agents should be part of the supportive periodontal therapy for aggressive periodontitis.
Acute periodontal lesions
Authors: Herrera David , Alonso Bettina , de Arriba Lorenzo , Santa Cruz Isabel , Serrano Cristina , Sanz Mariano 
Published: April 2014

AbstractThis review provides updates on acute conditions affecting the periodontal tissues, including abscesses in the periodontium, necrotizing periodontal diseases and other acute conditions that cause gingival lesions with acute presentation, such as infectious processes not associated with oral bacterial biofilms, mucocutaneous disorders and traumatic and allergic lesions. A periodontal abscess is clinically important because it is a relatively frequent dental emergency, it can compromise the periodontal prognosis of the affected tooth and bacteria within the abscess can spread and cause infections in other body sites. Different types of abscesses have been identified, mainly classified by their etiology, and there are clear differences between those affecting a pre‐existing periodontal pocket and those affecting healthy sites. Therapy for this acute condition consists of drainage and tissue debridement, while an evaluation of the need for systemic antimicrobial therapy will be made for each case, based on local and systemic factors. The definitive treatment of the pre‐existing condition should be accomplished after the acute phase is controlled. Necrotizing periodontal diseases present three typical clinical features: papilla necrosis, gingival bleeding and pain. Although the prevalence of these diseases is not high, their importance is clear because they represent the most severe conditions associated with the dental biofilm, with very rapid tissue destruction. In addition to bacteria, the etiology of necrotizing periodontal disease includes numerous factors that alter the host response and predispose to these diseases, namely HIV infection, malnutrition, stress or tobacco smoking. The treatment consists of superficial debridement, careful mechanical oral hygiene, rinsing with chlorhexidine and daily re‐evaluation. Systemic antimicrobials may be used adjunctively in severe cases or in nonresponding conditions, being the first option metronidazole. Once the acute disease is under control, definitive treatment should be provided, including appropriate therapy for the pre‐existing gingivitis or periodontitis. Among other acute conditions affecting the periodontal tissues, but not caused by the microorganisms present in oral biofilms, infectious diseases, mucocutaneous diseases and traumatic or allergic lesions can be listed. In most cases, the gingival involvement is not severe; however, these conditions are common and may prompt an emergency dental visit. These conditions may have the appearance of an erythematous lesion, which is sometimes erosive. Erosive lesions may be the direct result of trauma or a consequence of the breaking of vesicles and bullae. A proper differential diagnosis is important for adequate management of the case.
CladispaBaly: revision, biology and reassignment of the genus to the tribe Spilophorini (Coleoptera: Chrysomelidae: Cassidinae)
Authors: SEKERKA LUKÁŠ , WINDSOR DONALD , DURY GUILLAUME 
Published: April 2014

AbstractThe genus, Cladispa Baly 1858, is transferred from the tribe Imatidiini (= Cephaloleiini Chapuis, 1875) to Spilophorini Chapuis, 1875 based on the review of type material, newly collected specimens and molecular phylogenetic analysis. The type species, C. quadrimaculata Baly, 1858, is redescribed, and two new species, C. amboroensis sp.n. from Bolivia (Santa Cruz Department) and C. ecuadorica sp.n. from Ecuador (Pastaza Province), are described and figured. The morphology of C. amboroensis sp.n. immature stages is broadly consistent with other Spilophorini. Field observations document that both C. quadrimaculata and C. amboroensis sp.n. are trophic specialists on Orchideaceae. Keys to Cladispa species and Spilophorini genera are provided. Trophic associations of other Cassidinae and Orchideaceae are discussed.This published work has been registered in ZooBank,
http://zoobank.org/urn:lsid:zoobank.org:pub:42A1ECF3‐2030‐4938‐8F3D‐FE7EC36F303A
Abscisic acid inhibits root growth in Arabidopsis through ethylene biosynthesis
Authors: Luo Xingju , Chen Zhizhong , Gao Junping , Gong Zhizhong 
Published: April 2014

SummaryWhen first discovered in 1963, abscisic acid (ABA) was called abscisin II because it promotes abscission. Later, researchers found that ABA accelerates abscission via ethylene. In Arabidopsis, previous studies have shown that high concentrations of ABA inhibit root growth through ethylene signaling but not ethylene production. In the present study in Arabidopsis, we found that ABA inhibits root growth by promoting ethylene biosynthesis. The ethylene biosynthesis inhibitor L–α–(2‐aminoethoxyvinyl)‐glycine reduces ABA inhibition of root growth, and multiple mutants of ACS (1–aminocyclopropane‐1–carboxylate synthase) are more resistant to ABA in terms of root growth than the wild‐type is. Two ABA‐activated calcium‐dependent protein kinases, CPK4 and CPK11, phosphorylate the C–terminus of ACS6 and increase the stability of ACS6 in ethylene biosynthesis. Plants expressing an ACS6 mutant that mimics the phosphorylated form of ACS6 produce more ethylene than the wild‐type. Our results reveal an important mechanism by which ABA promotes ethylene production. This mechanism may be highly conserved among higher plants.
Iron deficiency in blood donors: a national cross‐sectional study
Authors: Salvin Hannah E. , Pasricha Sant‐Rayn , Marks Denese C. , Speedy Joanna 
Published: April 2014

BackgroundIron deficiency (ID) is an important consequence of blood donation. The epidemiology of this problem in the blood donor population was therefore studied to enable appropriate targeting of potential solutions to donor ID.Study Design and MethodsA nationally representative, cluster‐based cross‐sectional study of Australian blood donors was performed. Donors were eligible for inclusion if they fulfilled criteria for blood donation or were deferred due to low or falling hemoglobin. Ferritin was measured and demographic and donation data were collected.ResultsA total of 3094 blood donors were recruited, of which samples were collected from 3049 donors; 1873 had exclusively donated whole blood (WB only), 242 had exclusively made apheresis donations, and 530 had not donated (“new” donors) in the previous 24 months. The prevalence of ID in new female donors was 12.0% compared with 1.3% in males. The prevalence of ID in female WB‐only donors was 26.4%; it increased with donation frequency and decreased with age. The prevalence in male WB‐only donors was 6.3% with no evident change with age or donation frequency. The prevalence of ID in apheresis‐only donors (females 6.3%; males 2.2%) did not significantly exceed that of new donors nor did it change with donation frequency. Importantly, the risk of ID could not be satisfactorily predicted in an individual donor by his or her anemia status or with predictive modeling incorporating demographic and donation data.ConclusionID is especially prevalent in female, premenopausal, frequent WB donors. Strategies to combat ID should be implemented, specifically targeting this group.
A Quality Control Program within a Clinical Trial Consortium for PCR Protocols To Detect Plasmodium Species
Authors: Taylor Steve M. , Mayor Alfredo , Mombo-Ngoma Ghyslain , Kenguele Hilaire M. , Ouédraogo Smaïla , Ndam Nicaise Tuikue , Mkali Happy , Mwangoka Grace , Valecha Neena , Singh Jai Prakash Narayan , Clark Martha A. , Verweij Jaco J. , Adegnika Ayola Akim , Severini Carlo , Menegon Michela , Macete Eusebio , Menendez Clara , Cisteró Pau , Njie Fanta , Affara Muna , Otieno Kephas , Kariuki Simon , ter Kuile Feiko O. , Meshnick Steven R. 
Published: April 2014

ABSTRACT

Malaria parasite infections that are only detectable by molecular methods are highly prevalent and represent a potential transmission reservoir. The methods used to detect these infections are not standardized, and their operating characteristics are often unknown. We designed a proficiency panel of
Plasmodium
spp. in order to compare the accuracy of parasite detection of molecular protocols used by labs in a clinical trial consortium. Ten dried blood spots (DBSs) were assembled that contained
P. falciparum
,
P. vivax
,
P. malariae
, and
P. ovale
; DBSs contained either a single species or a species mixed with
P. falciparum
. DBS panels were tested in 9 participating laboratories in a masked fashion. Of 90 tests, 68 (75.6%) were correct; there were 20 false-negative results and 2 false positives. The detection rate was 77.8% (49/63) for
P. falciparum
, 91.7% (11/12) for
P. vivax
, 83.3% (10/12) for
P. malariae
, and 70% (7/10) for
P. ovale
. Most false-negative
P. falciparum
results were from samples with an estimated ≤5 parasites per μl of blood. Between labs, accuracy ranged from 100% to 50%. In one lab, the inability to detect species in mixed-species infections prompted a redesign and improvement of the assay. Most PCR-based protocols were able to detect
P. falciparum
and
P. vivax
at higher densities, but these assays may not reliably detect parasites in samples with low
P. falciparum
densities. Accordingly, formal quality assurance for PCR should be employed whenever this method is used for diagnosis or surveillance. Such efforts will be important if PCR is to be widely employed to assist malaria elimination efforts.
Profiling of
rpoB
Mutations and MICs for Rifampin and Rifabutin in Mycobacterium tuberculosis
Authors: Jamieson F. B. , Guthrie J. L. , Neemuchwala A. , Lastovetska O. , Melano R. G. , Mehaffy C. 
Published: April 2014

ABSTRACT

Resistance to rifampin (RIF) and rifabutin (RFB) in
Mycobacterium tuberculosis
is associated with mutations within an 81-bp region of the
rpoB
gene (RIF resistance-determining region [RRDR]). Previous studies have shown that certain mutations in this region are more likely to confer high levels of RIF resistance, while others may be found in phenotypically susceptible isolates. In this study, we sought to determine the relationship between the MICs of RIF and RFB and
rpoB
RRDR mutations in 32 multidrug-resistant (MDR), 4 RIF-monoresistant, and 5 susceptible
M. tuberculosis
clinical isolates. The MICs were determined using the MGIT 960 system. Mutations in the
rpoB
RRDR were determined by Sanger sequencing. RpoB proteins with mutations S531L (a change of S to L at position 531), S531W, H526Y, and H526D and the double mutation D516A-R529Q were associated with high MICs for RIF and RFB. Five isolates carrying the mutations L511P, H526L, H526N, and D516G-S522L were found to be susceptible to RIF. Several mutations were associated with resistance to RIF and susceptibility to RFB (F514FF, D516V, and S522L). Whole-genome sequencing of two MDR isolates without
rpoB
RRDR mutations revealed a mutation outside the RRDR (V146F; RIF MIC of 50 μg/ml). The implications of the polymorphisms identified in the second of these isolates in RIF resistance need to be further explored. Our study further establishes a correlation between the mutations and the MICs of RIF and, also, RFB in
M. tuberculosis
. Several
rpoB
mutations were identified in RIF- and RFB-susceptible isolates. The clinical significance of these findings requires further exploration. Until then, a combination of phenotypic and molecular testing is advisable for drug susceptibility testing.
Within-Host Whole-Genome Deep Sequencing and Diversity Analysis of Human Respiratory Syncytial Virus Infection Reveals Dynamics of Genomic Diversity in the Absence and Presence of Immune Pressure
Authors: Grad Yonatan H. , Newman Ruchi , Zody Michael , Yang Xiao , Murphy Ryan , Qu James , Malboeuf Christine M. , Levin Joshua Z. , Lipsitch Marc , DeVincenzo John 
Published: April 2014

ABSTRACT
Human respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract disease in infants and young children and an important respiratory pathogen in the elderly and immunocompromised. While population-wide molecular epidemiology studies have shown multiple cocirculating RSV genotypes and revealed antigenic and genetic change over successive seasons, little is known about the extent of viral diversity over the course of an individual infection, the origins of novel variants, or the effect of immune pressure on viral diversity and potential immune-escape mutations. To investigate viral population diversity in the presence and absence of selective immune pressures, we studied whole-genome deep sequencing of RSV in upper airway samples from an infant with severe combined immune deficiency syndrome and persistent RSV infection. The infection continued over several months before and after bone marrow transplant (BMT) from his RSV-immune father. RSV diversity was characterized in 26 samples obtained over 78 days. Diversity increased after engraftment, as defined by T-cell presence, and populations reflected variation mostly within the G protein, the major surface antigen. Minority populations with known palivizumab resistance mutations emerged after its administration. The viral population appeared to diversify in response to selective pressures, showing a statistically significant growth in diversity in the presence of pressure from immunity. Defining escape mutations and their dynamics will be useful in the design and application of novel therapeutics and vaccines. These data can contribute to future studies of the relationship between within-host and population-wide RSV phylodynamics.

IMPORTANCE
Human RSV is an important cause of respiratory disease in infants, the elderly, and the immunocompromised. RSV circulating in a community appears to change season by season, but the amount of diversity generated during an individual infection and the impact of immunity on this viral diversity has been unclear. To address this question, we described within-host RSV diversity by whole-genome deep sequencing in a unique clinical case of an RSV-infected infant with severe combined immunodeficiency and effectively no adaptive immunity who then gained adaptive immunity after undergoing bone marrow transplantation. We found that viral diversity increased in the presence of adaptive immunity and was primarily within the G protein, the major surface antigen. These data will be useful in designing RSV treatments and vaccines and to help understand the relationship between the dynamics of viral diversification within individual hosts and the viral populations circulating in a community.
Lack of Significant Elevation of Myeloid-Derived Suppressor Cells in Peripheral Blood of Chronically Hepatitis C Virus-Infected Individuals
Authors: Nonnenmann Julia , Stirner Renate , Roider Julia , Jung Maria C. , Schrödl Kathrin , Bogner Johannes R. , Draenert Rika 
Published: April 2014

ABSTRACT

Myeloid-derived suppressor cells (MDSC) are immature myeloid cells with immunosuppressive function. Compared to the level in healthy controls (HC), no elevation of MDSC in chronic hepatitis C (cHEP-C) patients was found, and there was no difference in MDSC based on genotype or viral load (
P
> 0.25). Moreover, MDSC of cHEP-C patients inhibited CD8 T cell function as efficiently as MDSC of HC did. Since we detected neither quantitative nor qualitative differences in MDSC of cHEP-C patients relative to those of HC, we postulate that MDSC in peripheral blood are most likely not significant regarding immune dysfunction in cHEP-C.
Enhanced Viral Replication and Modulated Innate Immune Responses in Infant Airway Epithelium following H1N1 Infection
Authors: Clay Candice C. , Reader J. Rachel , Gerriets Joan E. , Wang Theodore T. , Harrod Kevin S. , Miller Lisa A. 
Published: April 2014

ABSTRACTInfluenza is the cause of significant morbidity and mortality in pediatric populations. The contribution of pulmonary host defense mechanisms to viral respiratory infection susceptibility in very young children is poorly understood. As a surrogate to compare mucosal immune responses of infant and adult lungs, rhesus monkey primary airway epithelial cell cultures were infected with pandemic influenza A/H1N1 virusin vitro. Virus replication, cytokine secretion, cell viability, and type I interferon (IFN) pathway PCR array profiles were evaluated for both infant and adult cultures. In comparison with adult cultures, infant cultures showed significantly increased levels of H1N1 replication, reduced alpha interferon (IFN-α) protein synthesis, and no difference in cell death following infection. Age-dependent differences in expression levels of multiple genes associated with the type I IFN pathway were observed in H1N1-infected cultures. To investigate the pulmonary and systemic responses to H1N1 infection in early life, infant monkeys were inoculated with H1N1 by upper airway administration. Animals were monitored for virus and parameters of inflammation over a 14-day period. High H1N1 titers were recovered from airways at day 1, with viral RNA remaining detectable until day 9 postinfection. Despite viral clearance, bronchiolitis and alveolitis persisted at day 14 postinfection; histopathological analysis revealed alveolar septal thickening and intermittent type II pneumocyte hyperplasia. Our overall findings are consistent with the known susceptibility of pediatric populations to respiratory virus infection and suggest that intrinsic developmental differences in airway epithelial cell immune function may contribute to the limited efficacy of host defense during early childhood.IMPORTANCETo the best of our knowledge, this study represents the first report of intrinsic developmental differences in infant airway epithelial cells that may contribute to the increased susceptibility of the host to respiratory virus infections. Despite the global burden of influenza, there are currently no vaccine formulations approved for children <6 months of age. Given the challenges of conducting experimental studies involving pediatric patients, rhesus monkeys are an ideal laboratory animal model to investigate the maturation of pulmonary mucosal immune mechanisms during early life because they are most similar to those of humans with regard to postnatal maturation of the lung structure and the immune system. Thus, our findings are highly relevant to translational medicine, and these data may ultimately lead to novel approaches that enhance airway immunity in very young children.
Characteristics of Nucleocytoplasmic Transport of H1N1 Influenza A Virus Nuclear Export Protein
Authors: Gao Shengyan , Wang Shanshan , Cao Shuai , Sun Lei , Li Jing , Bi Yuhai , Gao George F. , Liu Wenjun 
Published: April 2014

ABSTRACT
The influenza A virus nuclear export protein (NEP) plays crucial roles in the nuclear export of the viral ribonucleoprotein complex through the chromosome region maintenance 1 (CRM1)-mediated cellular protein transport system. However, the detailed mechanism of NEP nucleocytoplasmic trafficking remains incompletely understood. Here, we investigated the subcellular localization of NEP from two strains of H1N1 influenza A virus and found that 2009 swine-origin H1N1 influenza A virus A/California/04/2009 (CA04) NEP displayed a distinct cellular distribution pattern, forming unique nuclear aggregates, compared to A/WSN/33 (H1N1) (WSN) NEP. Characterization of the nucleocytoplasmic transport pathways of these two NEPs showed that they both enter the nucleus by passive diffusion but are exported through the nuclear export receptor CRM1-mediated pathway with different efficiencies. The two identified nuclear export signals (NESs) on the two NEPs functioned similarly despite differences in their amino acid sequences. Using a two-hybrid assay, we confirmed that the CA04 NEP interacts less efficiently with CRM1 and that a threonine residue at position 48 is responsible for the nuclear aggregation. The present study revealed the dissimilarity in subcellular NEP transport processes between the 2009 pandemic (H1N1) influenza A virus CA04 and the laboratory-adapted H1N1 virus WSN and uncovered the mechanism responsible for this difference.

IMPORTANCE
Because the efficiency of the nucleocytoplasmic transport of viral components is often correlated with the viral RNA polymerase activity, propagation, and host range of influenza viruses, the present study investigated the subcellular localization of NEP from two strains of H1N1 influenza virus. We found that the NEPs of both A/California/04/2009 (H1N1) (CA04) and A/WSN/33 (H1N1) (WSN) enter the nucleus by passive diffusion but are exported with different efficiencies, which were caused by weaker binding activity between the CA04 NEP and CRM1. The results of the present study revealed characteristics of the nuclear import and export pathways of NEP and the mechanism responsible for the differences in the cellular distribution of NEP between two H1N1 strains.