bluuebunny/crossref_metadata_2025_split huggingface dataset:
The microRNA‐146a/b attenuates acute small‐for‐size liver graft injury in rats
Authors: Jiang Weiwei , Ni Qingfeng , Tan Longwei , Kong Liangliang , Lu Yeting , Xu Xiaoqun , Kong Lianbao 
Published: August 2014

AbstractBackground & AimsA critical role of the Toll‐like receptor (TLR)‐4 and its downstream mediators in the pathogenesis of small‐for‐size liver graft injury has been documented. Recently, the microRNA‐146 (miR‐146) was identified as a potent negative regulator of the TLR4 signalling pathway. In this study, the role of miR‐146a and miR‐146b in the attenuation of TLR‐4 signalling and small‐for‐size liver graft injury was investigated.MethodsThe expression levels of miR‐146a and miR‐146b during small‐for‐size liver graft injury were studied in vivo. In addition, the effects of miR‐146a and miR‐146b on the expression of IRAK1 and TRAF6 in the rat macrophage cell line NR8383 and rat liver kupffer cells were studied in vitro. The in vivo effect of miR‐146a and miR‐146b on small‐for‐size liver graft injury was studied by the tail vein injection of miR‐146a mimics and miR‐146b mimics.ResultsThe levels of miR‐146a and miR‐146b decreased with a small‐for‐size liver graft. MiR‐146a and miR‐146b inhibited IRAK1 and TRAF6 expression by binding to the 3′UTR of IRAK1 or TRAF6, respectively, in the rat macrophage cell line NR8383. The administration of miR‐146a mimics and miR‐146b mimics prevented liver graft injury in small‐for‐size liver graft injury via the inactivation of IRAK1 and TRAF6 in vivo.ConclusionsmiR‐146a and miR‐146b prevent liver injury in small‐for‐size liver graft injury via the inactivation of IRAK1 and TRAF6.
Branched‐chain amino acids reduce hepatic iron accumulation and oxidative stress in hepatitis C virus polyprotein‐expressing mice
Authors: Korenaga Masaaki , Nishina Sohji , Korenaga Keiko , Tomiyama Yasuyuki , Yoshioka Naoko , Hara Yuichi , Sasaki Yusuke , Shimonaka Yasushi , Hino Keisuke 
Published: August 2014

AbstractBackground & AimsBranched‐chain amino acids (BCAA) reduce the incidence of hepatocellular carcinoma (HCC) in patients with cirrhosis. However, the mechanisms that underlie these effects remain unknown. Previously, we reported that oxidative stress in male transgenic mice that expressed hepatitis C virus polyprotein (HCVTgM) caused hepatic iron accumulation by reducing hepcidin transcription, thereby leading to HCC development. This study investigated whether long‐term treatment with BCAA reduced hepatic iron accumulation and oxidative stress in iron‐overloaded HCVTgM and in patients with HCV‐related advanced fibrosis.MethodsMale HCVTgM were fed an excess‐iron diet that comprised either casein or 3.0% BCAA, or a control diet, for 6 months.ResultsFor HCVTgM, BCAA supplementation increased the serum hepcidin‐25 levels and antioxidant status [ratio of biological antioxidant potential (BAP) relative to derivatives of reactive oxygen metabolites (dROM)], decreased the hepatic iron contents, attenuated reactive oxygen species generation, and restored mitochondrial superoxide dismutase expression and mitochondrial complex I activity in the liver compared with mice fed the control diet. After 48 weeks of BCAA supplementation in patients with HCV‐related advanced fibrosis, BAP/dROM and serum hepcidin‐25 increased and serum ferritin decreased compared with the pretreatment levels.ConclusionsBCAA supplementation reduced oxidative stress by restoring mitochondrial function and improved iron metabolism by increasing hepcidin‐25 in both iron‐overloaded HCVTgM and patients with HCV‐related advanced fibrosis. These activities of BCAA may partially account for their inhibitory effects on HCC development in cirrhosis patients.
Liver inflammation is a risk factor for prediabetes in at‐risk latinos with and without hepatitis C infection
Authors: Burman Blaire E. , Bacchetti Peter , Ayala Claudia E. , Gelman Nicholas , Melgar Jennifer , Khalili Mandana 
Published: August 2014

AbstractBackground & AimsEarly recognition of prediabetes can lead to timely clinical interventions to prevent type 2 diabetes. Both Latino ethnicity and chronic hepatitis C (HCV) have been identified as diabetic risk factors. We aimed to investigate predictors of impaired fasting glucose (IFG), a common prediabetic state, among Latinos with and without HCV.MethodsOne hundred Latino adults with no history of diabetes or cirrhosis underwent clinical, laboratory, and metabolic evaluation, including oral glucose tolerance testing (OGTT) and insulin suppression testing to quantify directly measured insulin resistance (IR). Isolated IFG was defined as fasting glucose ≥100 mg/dl and <140 mg/dl at 2 h during normal glucose tolerance during OGTT.ResultsOverall subject characteristics included median age 44 years, 64% male, 40% HCV‐positive and 32% with isolated IFG. Factors associated with isolated IFG included subject age (OR 2.42 per decade, 95%CI 1.40–3.90, P = 0.001), HCV infection (OR 4.0, 95%CI 1.71–9.72, P = 0.002) and alanine aminotransferase (ALT) (OR 2.35 per doubling, 95%CI 1.46–3.77, P < 0.0001). Multipredictor logistic regression analysis identified ALT (OR 2.05 per doubling, P = 0.005, 95% CI 1.24–3.40) and age (OR 2.20 per 10 years, P = 0.005, 95%CI 1.27–3.80) as factors independently associated with IFG. While HCV was associated with 4‐fold higher odds of IFG, this entire effect was mediated by ALT.ConclusionsWe found strong evidence that liver inflammation is a risk factor for prediabetes among Latinos with and without HCV. Among HCV‐infected individuals, early antiviral therapy could mitigate the effect of inflammation and represent an important intervention to prevent diabetes in this at‐risk population.
Reduced Flow‐and Acetylcholine‐Induced Dilations in Visceral Compared to Subcutaneous Adipose Arterioles in Human Morbid Obesity
Authors: Grizelj Ivana , Cavka Ana , Bian Jing‐Tan , Szczurek Mary , Robinson Austin , Shinde Shruti , Nguyen Van , Braunschweig Carol , Wang Edward , Drenjancevic Ines , Phillips Shane A. 
Published: August 2014

AbstractBackground and AimsThe hypothesis of this study was that microvascular FID and AChID is impaired in visceral (VAT) compared to SAT arterioles in morbidly obese women. An Additional aim was to determine the mechanisms contributing to FID and AChID in VAT and SAT arterioles.Methods and ResultsArterioles were obtained from SAT and VAT biopsies from women (BMI > 35 kg/m2) undergoing bariatric surgery. Microvessels were cannulated for reactivity measurements in response to flow (pressure gradients of 10–100 cmH2O) and to ACh (10−9–10−4 M) with and without l‐NAME, INDO, and PEG‐catalase. NO and H2O2 generation were detected in arterioles by fluorescence microscopy. FID and AChID of arterioles from VAT were reduced compared to SAT arterioles. In SAT arterioles, l‐NAME, INDO, and PEG‐catalase significantly reduced FID and AChID but had no effect individually on VAT arterioles' vasodilator reactivity. INDO +l‐NAME reduced FID in VAT arterioles. NO‐fluorescence was greater in arterioles from SAT compared to VAT arterioles. Vascular H2O2 generation during flow was similar in both VAT and SAT.ConclusionOur results suggest that VAT arterioles display reduced vasodilator reactivity to flow and ACh compared to SAT arterioles, mediated by different regulatory mechanisms in human obesity.
Changes in dermal papilla structures due to aging in the facial cheek region
Authors: Mizukoshi K. , Yonekura K. , Futagawa M. , Nakamura T. , Hirayama K. , Takahashi K. 
Published: August 2014

Background/purposeIn the past, it has been possible to measure the dermal papilla structures which are undulations between the epidermis and dermis by noninvasive method. However, almost all of previous studies were not intended to measure facial skin but another site of body. Here, we investigated age‐dependent alterations for dermal papilla structures in the facial cheek region after elucidating the difference of characteristics between the body site.MethodsThe surface of the dermis was observed under scanning electron microscope (SEM) using face and abdominal skin biopsy samples. A total of 90 Japanese women were investigated by in vivo confocal laser microscope (CLSM). The number and the shape in the horizontal cross‐sectional images of the dermal papilla were analyzed.ResultsThe facial skin had different characteristics in comparison to the abdominal skin by SEM observation. Under CLSM observation, we found abnormal dermal papilla structures which were accompanied by spots or enlarged pore areas and eliminated these structures from our analysis. We revealed a decrease in the number of normal dermal papilla structures with age and large individual differences at younger ages.ConclusionWe found abnormal dermal papilla structures and differences in the dermal papilla structures between face and other body site. With these taken into consideration, we could precisely investigate the aging alteration of normal dermal papilla structures in the face.
A stearoyl‐acyl carrier protein desaturase, NbSACPD‐C, is critical for ovule development in Nicotiana benthamiana
Authors: Zhang Jiantao , Li Jianhui , Garcia‐Ruiz Hernan , Bates Philip D. , Mirkov Theodore Erik , Wang Xiaofeng 
Published: August 2014

SummaryStearoyl‐acyl carrier protein desaturase (SACPD) activity is essential for production of the major unsaturated fatty acids (UFAs) in plant lipids. We report here the characterization of three SACPD genes from Nicotiana benthamiana, NbSACPD‐A, ‐B, and ‐C. All three genes share high similarity to AtSSI2/FAB2 (Suppressor of Salicylic acid‐Insensitivity2/Fatty Acid Biosynthesis2), the primary SACPD isoform in Arabidopsis. Knocking down the expression of individual or combinations of NbSACPDs by an artificial microRNA approach resulted in significantly reduced accumulation of 18C UFAs and elevated levels of 18:0‐FA (Fatty acids) in leaves, indicating that all three genes participated in fatty acid desaturation. The triple knockdown (KD) plants displayed severe growth phenotypes, including spontaneous cell death and dwarfing. While no vegetative morphologic abnormality was observed in NbSACPD‐A, ‐B, or ‐C KD plants, strikingly, NbSACPD‐C KD plants produced small fruits with aborted ovules. Reciprocal crosses with wild‐type and NbSACPD‐C KD plants revealed that knocking down NbSACPD‐C expression caused female, but not male, sterility. Furthermore, arrested ovule development and significantly altered lipid composition in ovaries were observed in NbSACPD‐C KD plants, consistent with the predominant NbSACPD‐C expression in ovules. The ovule development defect was fully complemented by coexpressing an amiRNA‐resistant NbSACPD‐C variant in the NbSACPD‐C KD background, further supporting a specific requirement for NbSACPD‐C in female fertility. Our results thus indicated that NbSACPD‐C plays a critical role maintaining membrane lipid composition in ovule development for female fertility in N. benthamiana, complementing and extending prior understanding on the well‐demonstrated roles of SACPDs in biotic and abiotic stresses.
Arabidopsis inositol pentakisphosphate 2‐kinase, AtIPK1, is required for growth and modulates phosphate homeostasis at the transcriptional level
Authors: Kuo Hui‐Fen , Chang Tzu‐Yun , Chiang Su‐Fen , Wang Wei‐Di , Charng Yee‐yung , Chiou Tzyy‐Jen 
Published: August 2014

SummaryInositol hexakisphosphate (IP6) provides a phosphorous reservoir in plant seeds; in addition, along with its biosynthesis intermediates and derivatives, IP6 also plays important roles in diverse developmental and physiological processes. Disruption of the Arabidopsis inositol pentakisphosphate 2‐kinase coding gene AtIPK1 was previously shown to reduce IP6 content in vegetative tissues and affect phosphate (Pi) sensing. Here we show that AtIPK1 is required for sustaining plant growth, as null mutants are non‐viable. An incomplete loss‐of‐function mutant, atipk1‐1, exhibited disturbed Pi homeostasis and overaccumulated Pi as a consequence of increased Pi uptake activity and root‐to‐shoot Pi translocation. The atipk1‐1 mutants also showed a Pi deficiency‐like root system architecture with reduced primary root and enhanced lateral root growth. Transcriptome analysis indicated that a subset of Pi starvation‐responsive genes was transcriptionally perturbed in the atipk1‐1 mutants and the expression of multiple genes involved in Pi uptake, allocation, and remobilization was increased. Genetic and transcriptional analyses suggest that disturbance of Pi homeostasis caused by atipk1 mutation involved components in addition to PHR1(‐like) transcription factors. Notably, the transcriptional increase of a number of Pi starvation‐responsive genes in the atipk1‐1 mutants is correlated with the reduction of histone variant H2A.Z occupation in chromatin. The myo‐inositol‐1‐phosphate synthase mutants, atmips1 and atmips2 with comparable reduction in vegetative IP6 to that in the atipk1‐1 mutants did not overaccumulate Pi, suggesting that Pi homeostasis modulated by AtIPK1 is not solely attributable to IP6 level. This study reveals that AtIPK1 has important roles in growth and Pi homeostasis.
Arhodomonas sp. Strain Seminole and Its Genetic Potential To Degrade Aromatic Compounds under High-Salinity Conditions
Authors: Dalvi Sonal , Nicholson Carla , Najar Fares , Roe Bruce A. , Canaan Patricia , Hartson Steven D. , Fathepure Babu Z. 
Published: August 2014

ABSTRACT

Arhodomonas
sp. strain Seminole was isolated from a crude oil-impacted brine soil and shown to degrade benzene, toluene, phenol, 4-hydroxybenzoic acid (4-HBA), protocatechuic acid (PCA), and phenylacetic acid (PAA) as the sole sources of carbon at high salinity. Seminole is a member of the genus
Arhodomonas
in the class
Gammaproteobacteria
, sharing 96% 16S rRNA gene sequence similarity with
Arhodomonas aquaeolei
HA-1. Analysis of the genome predicted a number of catabolic genes for the metabolism of benzene, toluene, 4-HBA, and PAA. The predicted pathways were corroborated by identification of enzymes present in the cytosolic proteomes of cells grown on aromatic compounds using liquid chromatography-mass spectrometry. Genome analysis predicted a cluster of 19 genes necessary for the breakdown of benzene or toluene to acetyl coenzyme A (acetyl-CoA) and pyruvate. Of these, 12 enzymes were identified in the proteome of toluene-grown cells compared to lactate-grown cells. Genomic analysis predicted 11 genes required for 4-HBA degradation to form the tricarboxylic acid (TCA) cycle intermediates. Of these, proteomic analysis of 4-HBA-grown cells identified 6 key enzymes involved in the 4-HBA degradation pathway. Similarly, 15 genes needed for the degradation of PAA to the TCA cycle intermediates were predicted. Of these, 9 enzymes of the PAA degradation pathway were identified only in PAA-grown cells and not in lactate-grown cells. Overall, we were able to reconstruct catabolic steps for the breakdown of a variety of aromatic compounds in an extreme halophile, strain Seminole. Such knowledge is important for understanding the role of
Arhodomonas
spp. in the natural attenuation of hydrocarbon-impacted hypersaline environments.
Combined Use of Bacteriophage K and a Novel Bacteriophage To Reduce Staphylococcus aureus Biofilm Formation
Authors: Alves D. R. , Gaudion A. , Bean J. E. , Perez Esteban P. , Arnot T. C. , Harper D. R. , Kot W. , Hansen L. H. , Enright M. C. , Jenkins A. Tobias A. 
Published: August 2014

ABSTRACTBiofilms are major causes of impairment of wound healing and patient morbidity. One of the most common and aggressive wound pathogens isStaphylococcus aureus, displaying a large repertoire of virulence factors and commonly reduced susceptibility to antibiotics, such as the spread of methicillin-resistantS. aureus(MRSA). Bacteriophages are obligate parasites of bacteria. They multiply intracellularly and lyse their bacterial host, releasing their progeny. We isolated a novel phage, DRA88, which has a broad host range amongS. aureusbacteria. Morphologically, the phage belongs to theMyoviridaefamily and comprises a large double-stranded DNA (dsDNA) genome of 141,907 bp. DRA88 was mixed with phage K to produce a high-titer mixture that showed strong lytic activity against a wide range ofS. aureusisolates, including representatives of the major international MRSA clones and coagulase-negativeStaphylococcus. Its efficacy was assessed both in planktonic cultures and when treating established biofilms produced by three different biofilm-producingS. aureusisolates. A significant reduction of biofilm biomass over 48 h of treatment was recorded in all cases. The phage mixture may form the basis of an effective treatment for infections caused byS. aureusbiofilms.
Collagen-Like Glycoprotein BclS Is Involved in the Formation of Filamentous Structures of the Lysinibacillus sphaericus Exosporium
Authors: Zhao Ni , Ge Yong , Shi Tingyu , Hu Xiaomin , Yuan Zhiming 
Published: August 2014

ABSTRACT

Lysinibacillus sphaericus
produces mosquitocidal binary toxins (Bin toxins) deposited within a balloon-like exosporium during sporulation. Unlike
Bacillus cereus
group strains, the exosporium of
L. sphaericus
is usually devoid of the hair-like nap, an external filamentous structure formed by a collagen-like protein, BclA. In this study, a new collagen-like exosporium protein encoded by Bsph_0411 (BclS) from
L. sphaericus
C3-41 was characterized. Thin-section electron microscopy revealed that deletion of
bclS
resulted in the loss of the filamentous structures that attach to the exosporium basal layer and spread through the interspace of spores.
In vivo
visualization of BclS-green fluorescent protein (GFP)/mCherry fusion proteins revealed a dynamic pattern of fluorescence that encased the spore from the mother cell-distal (MCD) pole of the forespore, and the BclS-GFP fusions were found to be located in the interspace of the spore, as confirmed by three-dimensional (3D) superresolution fluorescence microscopy. Further studies demonstrated that the
bclS
mutant spores were more sensitive to wet-heat treatment and germinated at a lower rate than wild-type spores and that these phenotypes were significantly restored in the
bclS
-complemented strain. These results suggested novel roles of collagen-like protein in exosporium assembly and spore germination, providing a hint for a further understanding of the genetic basis of the high level of persistence of Bin toxins in nature.
Erythrocyte Lysis and Xenopus laevis Oocyte Rupture by Recombinant Plasmodium falciparum Hemolysin III
Authors: Moonah Shannon , Sanders Natalie G. , Persichetti Jason K. , Sullivan David J. 
Published: August 2014

ABSTRACT

Malaria kills more than 1 million people per year worldwide, with severe malaria anemia accounting for the majority of the deaths. Malaria anemia is multifactorial in etiology, including infected erythrocyte destruction and decrease in erythrocyte production, as well as destruction or clearance of noninfected erythrocytes. We identified a panspecies
Plasmodium
hemolysin type III related to bacterial hemolysins. The identification of a hemolysin III homologue in
Plasmodium
suggests a potential role in host erythrocyte lysis. Here, we report the first characterization of
Plasmodium falciparum
hemolysin III, showing that the soluble recombinant
P. falciparum
hemolysin III is a pore-forming protein capable of lysing human erythrocytes in a dose-, time-, and temperature-dependent fashion. The recombinant
P. falciparum
hemolysin III-induced hemolysis was partially inhibited by glibenclamide, a known channel antagonist. Studies with polyethylene glycol molecules of different molecular weights indicated a pore size of approximately 3.2 nm. Heterologous expression of recombinant
P. falciparum
hemolysin III in
Xenopus
oocytes demonstrated early hypotonic lysis similar to that of the pore-forming aquaporin control. Live fluorescence microscopy localized transfected recombinant green fluorescent protein (GFP)-tagged
P. falciparum
hemolysin III to the essential digestive vacuole of the
P. falciparum
parasite. These transfected trophozoites also possessed a swollen digestive vacuole phenotype. Native
Plasmodium
hemolysin III in the digestive vacuole may contribute to lysis of the parasitophorous vacuole membrane derived from the host erythrocyte. After merozoite egress from infected erythrocytes, remnant
P. falciparum
hemolysin III released from digestive vacuoles could potentially contribute to lysis of uninfected erythrocytes to contribute to severe life-threatening anemia.
Factors that are associated with the risk of acquiringPlasmodium knowlesimalaria in Sabah, Malaysia: a case-control study protocol
Authors: Grigg M J , William T , Drakeley C J , Jelip J , von Seidlein L , Barber B E , Fornace K M , Anstey N M , Yeo T W , Cox J 
Published: August 2014

IntroductionPlasmodium knowlesihas long been present in Malaysia, and is now an emerging cause of zoonotic human malaria. Cases have been confirmed throughout South-East Asia where the ranges of its natural macaque hosts andAnopheles leucosphyrusgroup vectors overlap. The majority of cases are from Eastern Malaysia, with increasing total public health notifications despite a concurrent reduction inPlasmodium falciparumandP. vivaxmalaria. The public health implications are concerning givenP. knowlesihas the highest risk of severe and fatal disease of allPlasmodiumspp in Malaysia. Current patterns of risk and disease vary based on vector type and competence, with individual exposure risks related to forest and forest-edge activities still poorly defined. Clustering of cases has not yet been systematically evaluated despite reports of peri-domestic transmission and known vector competence for human-to-human transmission.Methods and analysisA population-based case–control study will be conducted over a 2-year period at two adjacent districts in north-west Sabah, Malaysia. Confirmed malaria cases presenting to the district hospital sites meeting relevant inclusion criteria will be requested to enrol. Three community controls matched to the same village as the case will be selected randomly. Study procedures will include blood sampling and administration of household and individual questionnaires to evaluate potential exposure risks associated with acquisition ofP. knowlesimalaria. Secondary outcomes will include differences in exposure variables betweenP. knowlesiand otherPlasmodiumspp, risk of severeP. knowlesimalaria, and evaluation ofP. knowlesicase clustering. Primary analysis will be per protocol, with adjusted ORs for exposure risks between cases and controls calculated using conditional multiple logistic regression models.EthicsThis study has been approved by the human research ethics committees of Malaysia, the Menzies School of Health Research, Australia, and the London School of Hygiene and Tropical Medicine, UK.