bluuebunny/crossref_metadata_2025_split huggingface dataset:
Parenteral‐nutrition‐associated liver disease after intestinal perforation in extremely low‐birthweight infants: Consequent lethal portal hypertension
Authors: Kubota Akio , Mochizuki Narutaka , Shiraishi Jun , Nakayama Masahiro , Kawahara Hisayoshi , Yoneda Akihiro , Tazuke Yuko , Goda Taro , Nakahata Kengo , Sano Hiroyuki , Hirano Shinya , Kitajima Hiroyuki 
Published: December 2012

AbstractBackgroundParenteral nutrition (PN)‐associated liver dysfunction (PNALD) in term infants usually manifests as intrahepatic cholestasis, which recovers with enteral nutrition (EN) in most cases; however, as the number of extremely low‐birthweight infants (ELBWI) has been increasing, and consequently intestinal diseases associated with ELBWI have been increasing, more intractable PNALD has been encountered after surgical treatment in ELBWI, which does not resolve or rather worsens with EN.MethodsThree cases of ELBWI with intestinal perforation, which developed PNALD and eventually died of hepatic failure with intractable portal hypertension, were reviewed. Their gestational age and birthweight ranged from 23 to 26 weeks, and from 434 to 968 g, respectively. The intestinal diseases included necrotizing enteritis in two and meconium‐related ileus with focal intestinal perforation in one.ResultsThe duration of total PN without EN in the three cases was 17, 24 and 24 days, respectively. The interval between the introduction of PN and the onset of PNALD was 14, 4 and 18 days, respectively. A marked elevation of serum endotoxin level was detected in both cases of necrotizing enteritis. Histopathological study of the liver revealed marked cholestasis, significant hepatic necrosis with fibrosis, and proliferation of ductules in all these cases, which was responsible for portal hypertension.ConclusionsPN after gastrointestinal disorders in ELBWI may cause refractory PNALD, which does not resolve, or rather worsens with the resumption of EN. Portal hypertension secondary to hepatic necrosis may be responsible for the exacerbation with the resumption of EN.
Maternal Hypertensive Disorders during Pregnancy and Mild Cognitive Limitations in the Offspring
Authors: Heikura Ulla , Hartikainen Anna‐Liisa , Nordström Tanja , Pouta Anneli , Taanila Anja , Järvelin Marjo‐Riitta 
Published: December 2012

AbstractBackgroundIt remains unclear whether maternal hypertensive disorders could impact cognitive development of the child. The aim of this study was to explore the association between hypertensive disorders and other maternal biological and social factors on the risk of mild cognitive limitations (intelligence quotient 50–85) in the offspring.MethodsAn 11.5‐year follow‐up study of the Northern Finland Birth Cohort 1986 (n = 9432) was utilised. The analysis included 8847 singleton children, of whom 198 had mild cognitive limitations. Gestational hypertension was defined as de novo hypertension (blood pressure ≥ 140/90), diagnosed mid‐pregnancy in a previously normotensive woman. Data on intelligence level of the children were based on standardised intelligence test results.ResultsEleven per cent (n = 20) of mothers having a child with mild cognitive limitations had gestational hypertension. Maternal gestational hypertension was independently associated with increased odds of mild cognitive limitation in the offspring (odds ratio 2.4 [95% confidence interval 1.4, 3.9]). Other independent maternal risk factors for mild cognitive limitation were high pre‐pregnancy body mass index (≥30 kg/m2), multiparity (≥4) and low education. In addition family's socio‐economic status lower than professional, male gender and small birthweight‐for‐gestational age appeared as independent risk factors for mild cognitive limitation.ConclusionsGestational hypertension should be considered as one of the adverse early risk factors that may predispose to impaired cognitive development in childhood.
Historical perspective and better regulatory governance: An agenda for institutional reform
Authors: Balleisen Edward J. , Brake Elizabeth K. 
Published: December 2012

AbstractCompared to economics, sociology, political science, and law, the discipline of history has had a limited role in the wide‐ranging efforts to reconsider strategies of regulatory governance, especially inside regulatory institutions. This article explores how more sustained historical perspective might improve regulatory decisionmaking. We first survey how a set of American regulatory agencies currently rely on historical research and analysis, whether for the purposes of public relations or as a means of supporting policymaking. We then consider how regulatory agencies might draw on history more self‐consciously, more strategically, and to greater effect. Three areas stand out in this regard – the use of history to improve understanding of institutional culture; reliance on historical analysis to test the empirical plausibility of conceptual models that make assumptions about the likelihood of potential economic outcomes; and integration of historical research methods into program and policy evaluation.
Intra‐messinian gypsum palaeokarst in the Northern Apennines and its palaeogeographic implications
Authors: De Waele Jo , Pasini Giancarlo 
Published: December 2012

AbstractA short intra‐Messinian continental period has been recognised in some North Italian gypsum areas, mostly under the form of palaeokarst deposits. This emersion appears to have occurred only locally, and is explained as caused by the intra‐Messinian tectonic phase and a major sea level lowering. Evidences of this palaeokarst are mostly small, although at some places the palaeontological content of its fillings is of great importance. The discovery near Zola Predosa (Bologna) of a new intra‐Messinian extensive karst system and of its infilling sheds new light on the importance of this karst episode.
Association between a functional polymorphism in Toll‐like receptor 3 and chronic hepatitis C in liver transplant recipients
Authors: Lee S.‐O. , Brown R.A. , Razonable R.R. 
Published: December 2012

AbstractBackgroundToll‐like receptor 3 (TLR3) is implicated in the pathogenesis of viral diseases owing to its ability to recognize viral double‐stranded RNA. We hypothesized that single nucleotide polymorphism (SNP) in TLR3 gene that impairs the function of the protein‐receptor influences the outcome of hepatitis C virus (HCV) infection after liver transplantation.MethodsThe clinical characteristics of 611 liver recipients (HCV‐infected: n = 153, non‐HCV‐infected: n = 458) were assessed to investigate the impact of TLR3 L412F SNP on transplant outcomes.ResultsTLR3 L412F is common, and it was significantly more prevalent among the HCV‐infected cohort (57.5% vs. 45.2%, P = 0.008). In a multivariate analysis, TLR3 L412F was significantly associated with chronic hepatitis C (odds ratio: 1.73, 95% confidence interval [CI]: 1.13–2.65, P = 0.01). In an analysis that compared HCV‐infected patients with wild‐type versus TLR3 L412F, a marginally higher rate of allograft failure and mortality was observed in the TLR3 L412F group (44.3% vs. 30.8%, P = 0.09). However, in a multivariate analysis, only donor age was significantly associated with allograft failure and mortality (relative risk: 1.04, 95% CI: 1.007–1.06, P = 0.02).ConclusionTLR3 L412F is significantly common in HCV‐infected liver recipients, and may be associated with worse outcomes. However, larger studies are needed to determine its significant association with allograft failure and mortality after liver transplantation for chronic hepatitis C.
Bladder transitional cell carcinoma and BK virus in a young kidney transplant recipient
Authors: Pino L. , Rijo E. , Nohales G. , Frances A. , Ubre A. , Arango O. 
Published: December 2012

AbstractKidney transplant recipients have a heightened risk of developing neoplasms. Immunosuppressive treatments decrease the incidence of transplant rejection but increase the risk of infections, including BK virus (BKV). This infection is acquired in childhood and remains latent in the renal and urinary epithelium. In cases of immunodeficiency, BKV has been implicated as a tumor virus, but the role of BKV in cancer is a controversial topic and is difficult to determine. In the tumor cells, it is possible to detect fragments of the viral genome that could alter the control mechanisms of the cell cycle and DNA repair. We report the case of a kidney transplant recipient who developed BKV nephropathy and carcinoma of the bladder, supporting a possible role for BKV in the oncogenic pathway in this clinical setting, but the role of BKV in cancer remains a controversial topic and difficult to determine.
ATR and MKP1 play distinct roles in response to UV‐B stress in Arabidopsis
Authors: González Besteiro Marina A. , Ulm Roman 
Published: December 2012

SummaryUltraviolet‐B (UV‐B) stress activates MAP kinases (MAPKs) MPK3 and MPK6 in Arabidopsis. MAPK activity must be tightly controlled in order to ensure an appropriate cellular outcome. MAPK phosphatases (MKPs) effectively control MAPKs by dephosphorylation of phosphothreonine and phosphotyrosine in their activation loops. Arabidopsis MKP1 is an important regulator of MPK3 and MPK6, and mkp1 knockout mutants are hypersensitive to UV‐B stress, which is associated with reduced inactivation of MPK3 and MPK6. Here, we demonstrate that MPK3 and MPK6 are hyperactivated in response to UV‐B in plants that are deficient in photorepair, suggesting that UV‐damaged DNA is a trigger of MAPK signaling. This is not due to a block in replication, as, in contrast to atr, the mkp1 mutant is not hypersensitive to the replication‐inhibiting drug hydroxyurea, hydroxyurea does not activate MPK3 and MPK6, and atr is not impaired in MPK3 and MPK6 activation in response to UV‐B. We further show that mkp1 leaves and roots are UV‐B hypersensitive, whereas atr is mainly affected at the root level. Tolerance to UV‐B stress has been previously associated with stem cell removal and CYCB1;1 accumulation. Although UV‐B‐induced stem cell death and CYCB1;1 expression are not altered in mkp1 roots, CYCB1;1 expression is reduced in mkp1 leaves. We conclude that the MKP1 and ATR pathways operate in parallel, with primary roles for ATR in roots and MKP1 in leaves.
Aqueous humor fibrinolytic activity in dogs with cataracts
Authors: Escanilla Natàlia , Leiva Marta , Monreal Luís , Ríos José , Peña Teresa 
Published: December 2012

AbstractObjectiveTo investigate fibrinolytic activity in aqueous humor (AH) of healthy and sick dogs, with and without cataracts.ProcedureProspective observational clinical study. A total of 45 dogs were included in the study. Physical and ophthalmic examinations, complete blood cell count (CBC) and serum biochemistry panel were performed in all animals. According to the ocular and systemic diagnoses, animals were classified into three groups: sick dogs without cataracts (20 dogs; 40 eyes), diabetic dogs with cataracts (11 dogs; 22 eyes), and healthy dogs with cataracts (14 dogs; 25 eyes). Bilateral AH and blood samples were collected during intraocular surgery (25 dogs; 47 eyes), or immediately after euthanasia (20 dogs; 40 eyes). Citrated samples were centrifuged and stored at −81 °C until analysis. Plasma and AH D‐dimer concentration were determined using a quantitative immunoturbidimetric latex agglutination assay.ResultsA total of 108 canine samples (45 plasma and 87 AH samples) were obtained. D‐dimer concentration in log‐scale, in AH of eyes with diabetic cataract was significantly higher thanAHof eyes with nondiabetic cataract, with a difference of 0.9 ng/mL 95% confidence interval (CI) (0.2; 1.6)P = 0.0116 and higher than that of sick animals with healthy eyes, with a estimated difference of −0.89 ng/mL 95% CI (−1.52; −0.25)P = 0.0061.PlasmaD‐dimer concentration was significantly higher in the group of animals with systemic disease [median 606 ng/mL, Interquartil Range (IQR) 145–1956 ng/mL] than in healthy dogs (median 47.5 ng/mL, IQR 4–250 ng/mL) (P = 0.002) and diabetic dogs (median 60.5 ng/mL, IQR 0–147.5 ng/mL) (P < 0.001).ConclusionAH fibrinolysis is present in dogs, being significantly higher in animals with diabetic cataracts than in those without cataracts, and those with nondiabetic cataracts.
Evaluation of Protective Potential of Yersinia pestis Outer Membrane Protein Antigens as Possible Candidates for a New-Generation Recombinant Plague Vaccine
Authors: Erova Tatiana E. , Rosenzweig Jason A. , Sha Jian , Suarez Giovanni , Sierra Johanna C. , Kirtley Michelle L. , van Lier Christina J. , Telepnev Maxim V. , Motin Vladimir L. , Chopra Ashok K. 
Published: December 2012

ABSTRACT

Plague caused by
Yersinia pestis
manifests itself in bubonic, septicemic, and pneumonic forms. Although the U.S. Food and Drug Administration recently approved levofloxacin, there is no approved human vaccine against plague. The capsular antigen F1 and the low-calcium-response V antigen (LcrV) of
Y. pestis
represent excellent vaccine candidates; however, the inability of the immune responses to F1 and LcrV to provide protection against
Y. pestis
F1
−
strains or those which harbor variants of LcrV is a significant concern. Here, we show that the passive transfer of hyperimmune sera from rats infected with the plague bacterium and rescued by levofloxacin protected naive animals against pneumonic plague. Furthermore, 10 to 12 protein bands from wild-type (WT)
Y. pestis
CO92 reacted with the aforementioned hyperimmune sera upon Western blot analysis. Based on mass spectrometric analysis, four of these proteins were identified as attachment invasion locus (Ail/OmpX), plasminogen-activating protease (Pla), outer membrane protein A (OmpA), and F1. The genes encoding these proteins were cloned, and the recombinant proteins purified from
Escherichia coli
for immunization purposes before challenging mice and rats with either the F1
−
mutant or WT CO92 in bubonic and pneumonic plague models. Although antibodies to Ail and OmpA protected mice against bubonic plague when challenged with the F1
−
CO92 strain, Pla antibodies were protective against pneumonic plague. In the rat model, antibodies to Ail provided protection only against pneumonic plague after WT CO92 challenge. Together, the addition of
Y. pestis
outer membrane proteins to a new-generation recombinant vaccine could provide protection against a wide variety of
Y. pestis
strains.
Human Cytomegalovirus pUL29/28 and pUL38 Repression of p53-Regulated p21CIP1 and Caspase 1 Promoters during Infection
Authors: Savaryn John P. , Reitsma Justin M. , Bigley Tarin M. , Halligan Brian D. , Qian Zhikang , Yu Dong , Terhune Scott S. 
Published: December 2012

ABSTRACT
During infection by human cytomegalovirus (HCMV), the tumor suppressor protein p53, which promotes efficient viral gene expression, is stabilized. However, the expression of numerous p53-responsive cellular genes is not upregulated. The molecular mechanism used to manipulate the transcriptional activity of p53 during infection remains unclear. The HCMV proteins IE1, IE2, pUL44, and pUL84 likely contribute to the regulation of p53. In this study, we used a discovery-based approach to identify the protein targets of the HCMV protein pUL29/28 during infection. Previous studies have demonstrated that pUL29/28 regulates viral gene expression by interacting with the chromatin remodeling complex NuRD. Here, we observed that pUL29/28 also associates with p53, an additional deacetylase complex, and several HCMV proteins, including pUL38. We confirmed the interaction between p53 and pUL29/28 in both the presence and absence of infection. HCMV pUL29/28 with pUL38 altered the activity of the 53-regulatable p21CIP1 promoter. During infection, pUL29/28 and pUL38 contributed to the inhibition of p21CIP1 as well as caspase 1 expression. The expression of several other p53-regulating genes was not altered. Infection using a UL29-deficient virus resulted in increased p53 binding and histone H3 acetylation at the responsive promoters. Furthermore, expression of pUL29/28 and its interacting partner pUL38 contributed to an increase in the steady-state protein levels of p53. This study identified two additional HCMV proteins, pUL29/28 and pUL38, which participate in the complex regulation of p53 transcriptional activity during infection.
Estimating the Rate of Intersubtype Recombination in Early HIV-1 Group M Strains
Authors: Ward Melissa J. , Lycett Samantha J. , Kalish Marcia L. , Rambaut Andrew , Leigh Brown Andrew J. 
Published: December 2012

ABSTRACT

West Central Africa has been implicated as the epicenter of the HIV-1 epidemic, and almost all group M subtypes can be found there. Previous analysis of early HIV-1 group M sequences from Kinshasa in the Democratic Republic of Congo, formerly Zaire, revealed that isolates from a number of individuals fall in different positions in phylogenetic trees constructed from sequences from opposite ends of the genome as a result of recombination between viruses of different subtypes. Here, we use discrete ancestral trait mapping to develop a procedure for quantifying HIV-1 group M intersubtype recombination across phylogenies, using individuals'
gag
(p17) and
env
(gp41) subtypes. The method was applied to previously described HIV-1 group M sequences from samples obtained in Kinshasa early in the global radiation of HIV. Nine different p17 and gp41 intersubtype recombinant combinations were present in the data set. The mean number of excess ancestral subtype transitions (NEST) required to map individuals' p17 subtypes onto the gp14 phylogeny samples, compared to the number required to map them onto the p17 phylogenies, and vice versa, indicated that excess subtype transitions occurred at a rate of approximately 7 × 10
−3
to 8 × 10
−3
per lineage per year as a result of intersubtype recombination. Our results imply that intersubtype recombination may have occurred in approximately 20% of lineages evolving over a period of 30 years and confirm intersubtype recombination as a substantial force in generating HIV-1 group M diversity.
Identification of Novel Influenza A Virus Proteins Translated from PA mRNA
Authors: Muramoto Yukiko , Noda Takeshi , Kawakami Eiryo , Akkina Ramesh , Kawaoka Yoshihiro 
Published: December 2012

ABSTRACT
Many replication events are involved in the influenza A virus life cycle, and they are accomplished by different virus proteins with specific functions. However, because the size of the influenza virus genome is limited, the virus uses different mechanisms to express multiple viral proteins from a single gene segment. The M2 and NS2 proteins are produced by splicing, and several novel influenza A virus proteins, such as PB1-F2, PB1-N40, and PA-X, have recently been identified. Here, we identified novel PA-related proteins in influenza A virus-infected cells. These newly identified proteins are translated from the 11th and 13th in-frame AUG codons in the PA mRNA and are, therefore, N-terminally truncated forms of PA, which we named PA-N155 and PA-N182, respectively. The 11th and 13th AUG codons are highly conserved among influenza A viruses, and the PA-N155 and PA-N182 proteins were detected in cells infected with various influenza A viruses isolated from different host species, suggesting the expression of these N-truncated PAs is universal in nature among influenza A viruses. These N-truncated PAs did not show polymerase activity when expressed together with PB1 and PB2; however, mutant viruses lacking the N-truncated PAs replicated more slowly in cell culture and had lower pathogenicity in mice than did wild-type virus. These results suggest that these novel PA-related proteins likely possess important functions in the replication cycle of influenza A virus.
Effects of Defective Interfering RNA on Symptom Induction by, and Replication of, a Novel Partitivirus from a Phytopathogenic Fungus, Rosellinia necatrix
Authors: Chiba Sotaro , Lin Yu-Hsin , Kondo Hideki , Kanematsu Satoko , Suzuki Nobuhiro 
Published: December 2012

ABSTRACT

A novel mycovirus termed Rosellinia necatrix partitivirus 2 (RnPV2), isolated from a phytopathogenic fungus,
Rosellinina necatrix
strain W57, was molecularly and biologically characterized in both natural and experimental host fungi. Three double-stranded RNA (dsRNA) segments, dsRNA1, dsRNA2, and defective interfering dsRNA1 (DI-dsRNA1), whose sizes were approximately 2.0, 1.8, and 1.7 kbp, respectively, were detected in W57. While the dsRNA2 sequence, encoding the coat protein, was reported previously, dsRNA1 and DI-dsRNA1 were shown to encode competent and defective (truncated) RNA-dependent RNA polymerase, respectively. Artificial introduction of RnPV2 into an RNA silencing-defective, Dicer-like 2 knockout mutant (Δ
dcl-2
) of a nonnatural host,
Cryphonectria parasitica
(chestnut blight fungus), resulted in successful infection by the DI-dsRNA1-carrying and -free RnPV2. The DI-dsRNA1-free RnPV2 strain was characterized by a higher ratio of accumulation of the intact dsRNA1 to dsRNA2, enhanced replication and severer symptom expression, compared with the DI-carrying strain. These findings confirmed the nature of DI-dsRNA1 as a DI-RNA. Both viral strains replicated to higher levels in a Δ
dcl-2
mutant than in a wild-type
C. parasitica
fungal strain (EP155) and induced severe symptoms in the Δ
dcl-2
mutant but subtle symptoms in EP155, indicating that the host RNA silencing targets the partitivirus. No obvious phenotypic effects of infection by either virus strain were detected in the natural host fungus. These combined results represent the first example of a partitivirus with DI-RNA that alters viral symptom induction in a host-dependent manner.
Divergent associations of drinking frequency and binge consumption of alcohol with mortality within the same cohort
Authors: Graff-Iversen Sidsel , Jansen Mona Dverdal , Hoff Dominic Anthony , Høiseth Gudrun , Knudsen Gun Peggy , Magnus Per , Mørland Jørg , Normann Per Trygve , Næss Øyvind Erik , Tambs Kristian 
Published: December 2012

BackgroundObservational studies show beneficial effects of moderate alcohol drinking on all-cause and cardiovascular disease (CVD) mortality, while binge drinking has been linked with increased mortality. The aim of this study was to assess the associations of alcohol use with mortality in a population with a hybrid of drinking patterns.MethodParticipants in a population based cardiovascular health survey in Finnmark county in 1987–1988, aged 20–62 years, constituted the study cohort. Alcohol use was self-reported by use of questions on frequency of beer, wine and liquor intake, and one question on intake of around five drinks or more per occasion (binge drinking). Information on education, income and use of alcohol in an earlier and in a later survey was linked to the file. Mortality was assessed throughout 2009 by Cox regression, with adjustment for potential confounding factors. In the analysis of mortality by frequency of any alcohol use, we adjusted for binge consumption and vice versa.ResultsTwo opposite trends appeared: a higher all-cause mortality in both sexes, and higher CVD mortality in men, with increasing frequency of binge drinking, compared with non-bingers. Second, in both sexes low-frequent use of any alcohol was associated with lower all-cause and CVD mortality, compared with abstention. The combination of any use of alcohol at least weekly and binge consumption at least monthly was common, particularly in men.ConclusionsQuestions on drinking frequency and a specific question on binge drinking capture different effects of alcohol use on all-cause and CVD mortality.