bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysing Success in the Fight against Malnutrition in Peru
Authors: Acosta Andrés Mejía 
Published: July 2011

SummaryThe prevalence of underweight children worldwide fell from 31per cent in 1990 to 26 per cent in 2008 (UNICEF 2009). However, progress is still slow and very uneven. Half of the countries have made progress on hunger, but levels of malnutrition did not improve in 28 countries and got worse in 24. The case of Peru appears to be an encouraging exception to the rule. With the support of CARE and others organisations from civil society and the donor community, the Peruvian Government has generated the political momentum to overcome obstacles and create national coordination structures and mechanisms, increase public (and private) spending on programs to tackle malnutrition and align social programs with the national nutrition strategy (known as CRECER). This included adding conditionalities on taking children to regular growth monitoring in the Conditional Cash Transfer programme, JUNTOS. The international aid system has also aligned itself around CRECER. After ten years of almost no change in child chronic malnutrition (stunting) rates (25.8 per cent in 1996, and 22.9 per cent in 2005 – with rural rates moving from 40.4 per cent to 40.1 per cent), this change in strategy has started to lead to results: malnutrition rates fell to 17.9 per cent between 2005 and 2010, with reductions mainly occurring in rural areas where malnutrition rates are highest (from 40.1per cent in 2005 to 31.3 per cent in 2010) according to the Peruvian National Statistical Office (INEI). Over 130,000 children under five are now not chronically malnourished who would have been had rates not fallen. Indeed, there is a strong case to be made that these changes would not have occurred without the formation in early 2006 of the Child Nutrition Initiative, and its advocacy success in getting ten Presidential candidates to sign a commitment to reduce chronic malnutrition in children under five by 5 per cent in five years (‘5 by 5 by 5’), followed by the support provided subsequently to the new government to meet that commitment.This paper documents and systematises Peru's recent experience in tackling malnutrition. Through an intensive review of quantitative and qualitative evidence, it argues that success is not explained by the presence of favourable socioeconomic changes in Peru, and it explores the political determinants of success in three dimensions. Horizontally, it looks at government efforts to form policy coalitions across representatives of different government and non‐government agencies; it looks at the vertical integration of agencies and programmes between national, regional and municipal governments, and it analyses the allocation of government resources used to fund the government's nutrition effort.In closing, the paper identifies some salient challenges to ensure long term sustainability of the initiative and draws policy recommendations and knowledge sharing lessons that could be of use for Southern Governments, donor agencies and civil society organisations.
Bactericidal effects of a high‐power, red light‐emitting diode on two periodontopathic bacteria in antimicrobial photodynamic therapy in vitro
Authors: Umeda Makoto , Tsuno Akiko , Okagami Yoshihide , Tsuchiya Fumito , Izumi Yuichi , Ishikawa Isao 
Published: July 2011

AbstractAim:  Light‐emitting diodes have been investigated as new light activators for photodynamic therapy. We investigated the bactericidal effects of high‐power, red light‐emitting diodes on two periodontopathic bacteria in vitro.Methods:  A light‐emitting diode (intensity: 1100 mW/cm2, peak wavelength: 650 nm) was used to irradiate a bacterial solution for either 10 or 20 s. Bacterial solutions (Porphyromonas gingivalis or Aggregatibacter actinomycetemcomitans) at a concentration of 2.5 × 106 c.f.u./mL were mixed with an equal volume of either methylene blue or toluidine blue O (0–20 μg/mL) and added to titer plate wells. The plate wells were irradiated with red light‐emitting diode light from a distance of 22 or 40 mm. The contents were diluted, and 50 μL was smeared onto blood agar plates. After 1 week of culturing, bacterial c.f.u. were counted.Results:  The light‐emitting diode energy density was estimated to be approximately 4 and 8 J/cm2 after 10 and 20 s of irradiation, respectively. Red light‐emitting diode irradiation for 10 s from a distance of 22 mm, combined with methylene blue at concentrations >10 μg/mL, completely killed Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans.Conclusion:  High‐power, red light‐emitting diode irradiation with a low concentration of dye showed effective bactericidal effects against two periodontopathic bacteria.
Therapeutic effect of topical ozonated oil on the epithelial healing of palatal wound sites: a planimetrical and cytological study
Authors: Patel Punit Vaibhav , Kumar Veerendra , Kumar Sheela , GD Vidya , Patel Amrita 
Published: July 2011

AbstractAim:  To evaluate the effect of ozonated oil on palatal wounds.Methods:  Eighteen patients were randomized and allocated to either the ozone group (n = 8) or control (n = 10) group. Free gingival graft surgery was performed, and post‐harvested palatal wounds were treated with either 2 mL ozonated oil or control oil daily for 1 week. A planimetrical analysis analyzed the digital image for the wound sizes and shape factor at baseline, at 24 h, and days 5, 7, 14, 21, and 28, postoperatively. A cytological analysis used the keratinization and superficial cell indices at baseline, 24 h, and days 3, 7, 14, and 21 and the second and third months, postoperatively.Results:  Planimetrical results showed a significant (P ≤ 0.05) improvement in wound size on days 5, 7, 14, 21, and 28, postoperatively, in the ozone group compared to the control group. Cytological results showed a significant (P ≤ 0.001) improvement in epithelial healing on days 7, 14, and 21, and the second and third months, postoperatively, after the application of ozonated oil compared to control oil.Conclusion:  Our results showed significant improvement in wound size and epithelial healing after topical ozonated oil application compared to control oil on palatal wounds.
Do dental implants preserve and maintain alveolar bone?
Authors: O’Neill Jessica E. , Yeung Stephen C. 
Published: July 2011

AbstractDental implants have been touted as capable of playing an active role in the maintenance of alveolar bone height, despite the lack of a sound biological basis to support this proposition. This paper reviews the biology of bone loss, the literature concerning alveolar bone remodeling in both the postextraction period and long term, and discusses the literature regarding the influence dental implant placement has on this process. Based on current evidence, implants do not have an active role in the preservation and maintenance of alveolar bone height. Following extraction of a tooth, no external influence has been identified that will prevent loss of bundle bone or alveolar bone remodeling. Additionally, the magnitude of change is patient, site, and time dependant. Further supporting evidence is required before it can be concluded that dental implants are capable of influencing alveolar bone remodeling.
Oral Treatment of Chickens with Lactobacilli Influences Elicitation of Immune Responses
Authors: Brisbin Jennifer T. , Gong Joshua , Orouji Shahriar , Esufali Jessica , Mallick Amirul I. , Parvizi Payvand , Shewen Patricia E. , Sharif Shayan 
Published: July 2011

ABSTRACTCommensal microbes in the intestine are in constant interaction with host cells and play a role in shaping the immune system.Lactobacillus acidophilus,Lactobacillus reuteri, andLactobacillus salivariusare members of the chicken intestinal microbiota and have been shown to induce different cytokine profiles in mononuclear cellsin vitro. The objective of the present study was to examine the effects of these bacteria individually or in combination on the induction of antibody- and cell-mediated immune responsesin vivo. The birds received lactobacilli weekly via oral gavage starting on day of hatch and subsequently, at 14 and 21 days, were immunized with sheep red blood cells (SRBC), keyhole limpet hemocyanin (KLH), Newcastle disease virus vaccine, and infectious bursal disease virus vaccine. Antibody responses in serum were measured weekly for 4 weeks beginning on the day of primary immunization. The cell-mediated immune response was evaluated at 21 days postimmunization by measurement of gamma interferon (IFN-γ) production in splenocytes stimulated with inactivated vaccine antigens.L. salivarius-treated birds had significantly more serum antibody to SRBC and KLH than birds that were not treated with probiotics.L. salivarius-treated birds also had decreased cell-mediated immune responses to recall antigen stimulation.L. reuteritreatment did not significantly affect the systemic immune response, whileL. acidophilustreatment increased the antibody response to KLH. These results indicate that systemic antibody- and cell-mediated immune responses can be modulated by oral treatment with lactobacilli but that these bacteria may vary in their ability to modulate the immune response.
Contribution of E3-Ubiquitin Ligase Activity to HIV-1 Restriction by TRIM5α
rh
: Structure of the RING Domain of TRIM5α
Authors: Lienlaf Maritza , Hayashi Fumiaki , Di Nunzio Francesca , Tochio Naoya , Kigawa Takanori , Yokoyama Shigeyuki , Diaz-Griffero Felipe 
Published: July 2011

ABSTRACT

TRIM5α
rh
is a cytosolic protein that potently restricts HIV-1 before reverse transcription. TRIM5α
rh
is composed of four different domains: RING, B-box 2, coiled coil, and B30.2(SPRY). The contribution of each of these domains to restriction has been extensively studied, with the exception of the RING domain. The RING domain of TRIM5α exhibits E3-ubiquitin ligase activity, but the contribution of this activity to the restriction of HIV-1 is not known. To test the hypothesis that the E3-ubiquitin ligase activity of the RING domain modulates TRIM5α
rh
restriction of HIV-1, we correlated the E3-ubiquitin ligase activity of a panel of TRIM5α
rh
RING domain variants with the ability of these mutant proteins to restrict HIV-1. For this purpose, we first solved the nuclear magnetic resonance structure of the RING domain of TRIM5α and defined potential functional regions of the RING domain by homology to other RING domains. With this structural information, we performed a systematic mutagenesis of the RING domain regions and tested the TRIM5α RING domain variants for the ability to undergo self-ubiquitylation. Several residues, particularly the ones on the E2-binding region of the RING domain, were defective in their self-ubiquitylation ability. To correlate HIV-1 restriction to self-ubiquitylation, we used RING domain mutant proteins that were defective in self-ubiquitylation but preserve important properties required for potent restriction by TRIM5α
rh
, such as capsid binding and higher-order self-association. From these investigations, we found a set of residues that when mutated results in TRIM5α molecules that lost both the ability to potently restrict HIV-1 and their self-ubiquitylation activity. Remarkably, all of these changes were in residues located in the E2-binding region of the RING domain. Overall, these results demonstrate a role for TRIM5α self-ubiquitylation in the ability of TRIM5α to restrict HIV-1.
Nuclear Accumulation of the Papillomavirus E1 Helicase Blocks S-Phase Progression and Triggers an ATM-Dependent DNA Damage Response
Authors: Fradet-Turcotte Amélie , Bergeron-Labrecque Fanny , Moody Cary A. , Lehoux Michaël , Laimins Laimonis A. , Archambault Jacques 
Published: July 2011

ABSTRACT
Replication of the papillomavirus genome is initiated by the assembly of a complex between the viral E1 and E2 proteins at the origin. The E1 helicase is comprised of a C-terminal ATPase/helicase domain, a central domain that binds to the origin, and an N-terminal regulatory region that contains nuclear import and export signals mediating its nucleocytoplasmic shuttling. We previously reported that nuclear accumulation of E1 has a deleterious effect on cellular proliferation which can be prevented by its nuclear export. Here we have shown that nuclear accumulation of E1 from different papillomavirus types blocks cell cycle progression in early S phase and triggers the activation of a DNA damage response (DDR) and of the ATM pathway in a manner that requires both the origin-binding and ATPase activities of E1. Complex formation with E2 reduces the ability of E1 to induce a DDR but does not prevent cell cycle arrest. Transient viral DNA replication still occurs in S-phase-arrested cells but surprisingly is neither affected by nor dependent on induction of a DDR and of the ATM kinase. Finally, we provide evidence that a DDR is also induced in human papillomavirus type 31 (HPV31)-immortalized keratinocytes expressing a mutant E1 protein defective for nuclear export. We propose that nuclear export of E1 prevents cell cycle arrest and the induction of a DDR during the episomal maintenance phase of the viral life cycle and that complex formation with E2 further safeguards undifferentiated cells from undergoing a DDR when E1 is in the nucleus.
Amino Acid Residues 253 and 591 of the PB2 Protein of Avian Influenza Virus A H9N2 Contribute to Mammalian Pathogenesis
Authors: Mok Chris Ka Pun , Yen Hui Ling , Yu May Yan Mei , Yuen Kit Man , Sia Sin Fun , Chan Michael Chi Wai , Qin Gang , Tu Wen Wei , Peiris Joseph Sriyal Malik 
Published: July 2011

ABSTRACT

We investigated the tropism, host responses, and virulence of two variants of A/Quail/Hong Kong/G1/1997 (H9N2) (H9N2/G1) with D253N and Q591K in the PB2 protein in primary human macrophages and bronchial epithelium
in vitro
and in mice
in vivo
. Virus with PB2 D253N and Q591K had greater polymerase activity in minireplicon assays, induced more tumor necrosis factor alpha (TNF-α) in human macrophages, replicated better in differentiated normal human bronchial epithelial (NHBE) cells, and was more pathogenic for mice. Taken together, our studies help define the viral genetic determinants that contribute to pathogenicity of H9N2 viruses.
High Cell-Free Virus Load and Robust Autologous Humoral Immune Responses in Breast Milk of Simian Immunodeficiency Virus-Infected African Green Monkeys
Authors: Wilks Andrew B. , Perry James R. , Ehlinger Elizabeth P. , Zahn Roland C. , White Robert , Gauduin Marie-Claire , Carville Angela , Seaman Michael S. , Schmitz Joern E. , Permar Sallie R. 
Published: July 2011

ABSTRACT

The design of immunologic interventions to prevent postnatal transmission of human immunodeficiency virus (HIV) will require identification of protective immune responses in this setting. Simian immunodeficiency virus (SIV)-infected rhesus monkeys (RMs), a species that develops an AIDS-like illness following experimental infection, transmit the virus at a high rate during breastfeeding. In contrast, postnatal transmission of SIV occurs rarely or not at all in natural, asymptomatic primate hosts of SIV. These contrasting transmission patterns provide a unique opportunity to study mechanisms that evolved to protect suckling infants from SIV infection. We compared the virologic and immunologic properties of milk of SIV-infected and uninfected natural hosts of SIV, African green monkeys (AGMs), to that of RMs. Interestingly, despite a low number of milk CD4
+
T lymphocytes in uninfected AGMs, milk virus RNA load in SIV-infected AGMs was comparable to that of SIV-infected RMs and that in AGM plasma. This observation is in contrast to the relatively low virus load in milk compared to that in plasma of SIV-infected RMs and HIV-infected women. Milk of SIV-infected AGMs also displayed robust virus-specific cellular immune responses. Importantly, an autologous challenge virus-specific neutralization response was detected in milk of five of six SIV-infected AGMs that was comparable in magnitude to that in plasma. In contrast, autologous challenge virus neutralization was not detectable in milk of SIV-infected RMs. The autologous virus-specific adaptive immune responses in breast milk of AGMs may contribute to impedance of virus transmission in the infant oral/gastrointestinal tract and the rarity of postnatal virus transmission in natural hosts of SIV.
Evidence for a Dual Antiviral Role of the Major Nuclear Domain 10 Component Sp100 during the Immediate-Early and Late Phases of the Human Cytomegalovirus Replication Cycle
Authors: Tavalai Nina , Adler Martina , Scherer Myriam , Riedl Yvonne , Stamminger Thomas 
Published: July 2011

ABSTRACT

In recent studies, the nuclear domain 10 (ND10) components PML and hDaxx were identified as cellular restriction factors that inhibit the initiation of human cytomegalovirus (HCMV) replication. The antiviral function of ND10, however, is antagonized by the IE1 protein, which induces ND10 disruption. Here we show that IE1 not only de-SUMOylates PML immediately upon infection but also directly targets Sp100. IE1 expression alone was sufficient to downregulate endogenous Sp100 independently of the presence of PML. Moreover, cotransfection experiments revealed that IE1 negatively interferes with the SUMOylation of all Sp100 isoforms. The modulation of Sp100 at immediate-early (IE) times of infection, indeed, seemed to have an
in vivo
relevance for HCMV replication, since knockdown of Sp100 resulted in more cells initiating the viral gene expression program. In addition, we observed that Sp100 was degraded in a proteasome-dependent manner at late times postinfection, suggesting that Sp100 may play an additional antiviral role during the late phase. Infection experiments conducted with Sp100 knockdown human foreskin fibroblasts (HFFs) confirmed this hypothesis: depletion of Sp100 resulted in augmented release of progeny virus particles compared to that from control cells. Consistent with this observation, we noted increased amounts of viral late gene products in the absence of Sp100. Importantly, this elevated late gene expression was not dependent on enhanced viral IE gene expression. Taken together, our data provide evidence that Sp100 is the first ND10-related factor identified that not only possesses the potential to restrict the initial stage of infection but also inhibits HCMV replication during the late phase.
The Histone Acetyltransferase CLOCK Is an Essential Component of the Herpes Simplex Virus 1 Transcriptome That Includes TFIID, ICP4, ICP27, and ICP22
Authors: Kalamvoki Maria , Roizman Bernard 
Published: July 2011

ABSTRACT
Studies published elsewhere have shown that the herpes simplex virus regulatory protein ICP0 interacts with BMAL1, a partner and regulator of circadian histone acetyltransferase CLOCK, that both proteins localize at ND10 bodies and are stabilized by viral proteins, that enzymatically active CLOCK partially complements ΔICP0 mutants, and that silencing of CLOCK suppresses the expression of viral genes. Here we report that CLOCK is a component of the transcriptional complex that includes TFIID, ICP4, ICP27, and ICP22. The results suggest that the CLOCK histone acetyltransferase is a component of the viral transcriptional machinery throughout the replicative cycle of the virus and that ICP27 and ICP22 initiate their involvement in viral gene expression as components of viral transcriptome.
Antigenic Drift in H5N1 Avian Influenza Virus in Poultry Is Driven by Mutations in Major Antigenic Sites of the Hemagglutinin Molecule Analogous to Those for Human Influenza Virus
Authors: Cattoli Giovanni , Milani Adelaide , Temperton Nigel , Zecchin Bianca , Buratin Alessandra , Molesti Eleonora , Aly Mona Meherez , Arafa Abdel , Capua Ilaria 
Published: July 2011

ABSTRACT
H5N1 highly pathogenic avian influenza virus has been endemic in poultry in Egypt since 2008, notwithstanding the implementation of mass vaccination and culling of infected birds. Extensive circulation of the virus has resulted in a progressive genetic evolution and an antigenic drift. In poultry, the occurrence of antigenic drift in avian influenza viruses is less well documented and the mechanisms remain to be clarified. To test the hypothesis that H5N1 antigenic drift is driven by mechanisms similar to type A influenza viruses in humans, we generated reassortant viruses, by reverse genetics, that harbored molecular changes identified in genetically divergent viruses circulating in the vaccinated population. Parental and reassortant phenotype viruses were antigenically analyzed by hemagglutination inhibition (HI) test and microneutralization (MN) assay. The results of the study indicate that the antigenic drift of H5N1 in poultry is driven by multiple mutations primarily occurring in major antigenic sites at the receptor binding subdomain, similarly to what has been described for human influenza H1 and H3 subtype viruses.
Suppression of STAT-1 Expression by Human Papillomaviruses Is Necessary for Differentiation-Dependent Genome Amplification and Plasmid Maintenance
Authors: Hong Shiyuan , Mehta Kavi P. , Laimins Laimonis A. 
Published: July 2011

ABSTRACTHigh-risk human papillomaviruses (HPVs) infect stratified epithelia to establish persistent infections that maintain low-copy-number episomes in infected basal cells. Amplification of viral genomes occurs upon keratinocyte differentiation, followed by virion synthesis. During persistent HPV infections, viral proteins act to evade surveillance by both innate and adaptive immune responses. One of the primary pathways regulating the innate immune response is the JAK/STAT pathway. Our studies indicate that the expression of STAT-1, but not other members of interferon (IFN)-stimulated gene factor 3 (ISGF-3) complex such as STAT-2 and IFN regulatory factor 9 (IRF9), is selectively suppressed by HPV proteins at the level of transcription. Both E6 and E7 oncoproteins independently suppress the expression of STAT-1, and mutational analyses indicate that the E6 targeting E6-associated protein (E6AP) is responsible for suppression. The levels of STAT-1 proteins increase upon differentiation of both normal and HPV-positive cells but are still significantly reduced in the latter cells. Transient restoration of STAT-1 levels in HPV-positive cells using recombinant retroviruses significantly impaired viral amplification upon differentiation while long-term increases abrogated maintenance of episomes. Similarly, increased levels of STAT-1 induced by gamma interferon treatment inhibited HPV genome amplification upon differentiation. Overall, our findings demonstrate that suppression of STAT-1 expression by HPV proteins is necessary for genome amplification and maintenance of episomes, suggesting an important role for this activity in viral pathogenesis.
The TRIM5α Genotype of Rhesus Macaques Affects Acquisition of Simian Immunodeficiency Virus SIVsmE660 Infection after Repeated Limiting-Dose Intrarectal Challenge
Authors: Reynolds Matthew R. , Sacha Jonah B. , Weiler Andrea M. , Borchardt Gretta J. , Glidden Chrystal E. , Sheppard Neil C. , Norante Francesca A. , Castrovinci Philip A. , Harris Jacqueline J. , Robertson Henry T. , Friedrich Thomas C. , McDermott Adrian B. , Wilson Nancy A. , Allison David B. , Koff Wayne C. , Johnson Welkin E. , Watkins David I. 
Published: July 2011

ABSTRACT

It has recently been shown that polymorphism at the rhesus macaque
TRIM5
locus can affect simian immunodeficiency virus (SIV) replication. Here we show that
TRIM5
alleles can also affect acquisition of SIVsmE660. Animals coexpressing the
TRIM5

TFP

and
TRIM5

CypA

alleles took significantly longer to become infected with SIVsmE660, but not SIVmac239, after repeated limiting-dose intrarectal challenge than did animals expressing other
TRIM5
allele combinations. Our results indicate that the
TRIM5
alleles can be a barrier to productive infection and that this should be taken into account when designing acquisition studies using SIVsmE660 or related viruses.