bluuebunny/crossref_metadata_2025_split huggingface dataset:
Population-Based Surveillance of Clostridium difficile Infection in Manitoba, Canada, by Using Interim Surveillance Definitions
Authors: Lambert Pascal J. , Dyck Myrna , Thompson Laura H. , Hammond Greg W. 
Published: September 2009

Objective.TO apply interim surveillance definitions of Clostridium difficile infection (CDI) cases to 1 year of data from the provincewide surveillance system of Manitoba, Canada, to determine the epidemiology of CDI incident cases in a population.Methods.CDI cases were categorized with interim surveillance definitions developed by an ad hoc C. difficile surveillance working group. Incident cases recorded in the provincial CDI database between July 2005 and June 2006 were linked to the provincial hospitalization and nursing home databases and analyzed.Results.One thousand six incident cases were identified over 1 year. Five hundred fifteen (51%) cases were associated with and began in a healthcare facility (HCF), whereas 275 (27%) were associated with and began in the community. An additional 131 (13%) cases were HCF associated but began in the community, while 85 (8%) were of indeterminate origin. Cases of HCF-associated CDI occurred in patients who were older than did cases of community-associated CDI (P < .0001). The provincial rate of community-onset cases was 23.4 per 100,000 person-years, and rates varied among geographic areas. HCF-associated CDI rates among the 10 largest hospitals varied from 0.5 to 8.4 per 10,000 patient-days. The time to CDI onset after hospital admission indicated that 25% of nosocomial cases began by the 8th day, and 50% began by the 17th day.Conclusions.Although the majority of CDI cases were associated with exposure to a HCF, 40% of incident CDI began in the community. Populations with HCF- and community-associated CDI demonstrated significantly different age distributions. The wide variation of rates among HCFs requires explanation. The high percentage of incident cases in the community warrants increased study.
STELLAR AND TOTAL BARYON MASS FRACTIONS IN GROUPS AND CLUSTERS SINCE REDSHIFT 1*
Authors: Giodini S. , Pierini D. , Finoguenov A. , Pratt G. W. , Boehringer H. , Leauthaud A. , Guzzo L. , Aussel H. , Bolzonella M. , Capak P. , Elvis M. , Hasinger G. , Ilbert O. , Kartaltepe J. S. , Koekemoer A. M. , Lilly S. J. , Massey R. , McCracken H. J. , Rhodes J. , Salvato M. , Sanders D. B. , Scoville N. Z. , Sasaki S. , Smolcic V. , Taniguchi Y. , Thompson D. 
Published: September 2009

ABSTRACT
We investigate if the discrepancy between estimates of the total baryon mass fraction obtained from observations of the cosmic microwave background (CMB) and of galaxy groups/clusters persists when a large sample of groups is considered. To this purpose, 91 candidate X-ray groups/poor clusters at redshift 0.1 ⩽ z ⩽ 1 are selected from the COSMOS 2 deg2 survey, based only on their X-ray luminosity and extent. This sample is complemented by 27 nearby clusters with a robust, analogous determination of the total and stellar mass inside R
500. The total sample of 118 groups and clusters with z ⩽ 1 spans a range in M
500 of ∼1013–1015
M
☉. We find that the stellar mass fraction associated with galaxies at R
500 decreases with increasing total mass as M
−0.37 ± 0.04
500, independent of redshift. Estimating the total gas mass fraction from a recently derived, high-quality scaling relation, the total baryon mass fraction (f
stars+gas
500 = f
stars
500 + f
gas
500) is found to increase by ∼25%, when M
500 increases from 〈M〉 = 5 × 1013
M
☉ to 〈M〉 = 7 × 1014
M
☉. After consideration of a plausible contribution due to intracluster light (11%–22% of the total stellar mass) and gas depletion through the hierarchical assembly process (10% of the gas mass), the estimated values of the total baryon mass fraction are still lower than the latest CMB measure of the same quantity (WMAP5), at a significance level of 3.3σ for groups of 〈M〉 = 5 × 1013
M
☉. The discrepancy decreases toward higher total masses, such that it is 1σ at 〈M〉 = 7 × 1014
M
☉. We discuss this result in terms of nongravitational processes such as feedback and filamentary heating.
Characterization of Resistant Starch Samples Prepared from Two High‐Amylose Maize Starches Through Debranching and Heat Treatments
Authors: Ozturk Serpil , Koksel Hamit , Ng Perry K. W. 
Published: September 2009

ABSTRACTThe aim of the present study was to investigate effects of debranching, autoclaving‐storing cycles, and drying processes (oven‐drying or freeze‐drying) on RS contents, thermal, pasting, and functional properties of high‐amylose maize starches (Hylon V and Hylon VII). The resistant starch (RS) contents increased (≤57.8%) with increasing autoclaving‐storing cycles. RS contents of oven‐dried samples were higher than those of freeze‐dried samples due to ongoing retrogradation of starch during oven drying at 50°C. Debranching caused a significant decrease in peak transition temperature and enthalpy values as compared with native starches. Solubility and water binding values of RS preparations were higher than those of native starches. Addition of native and autoclaved samples had improving effect on emulsion properties of albumin. Cold viscosity values of oven‐dried samples were lower as compared with freeze‐dried samples; this might be due to higher number of H‐bonds in the oven‐dried samples expected to be formed during drying. Debranching and autoclaving‐storing cycles caused decreases in peak, breakdown, and final viscosity values. The results of present study showed that debranching and heat treatments increased the RS contents and improved the functional properties of high‐amylose maize starches.
Effect of Temperature and Steeping Time on Calcium and Phosphorus Content in Nixtamalized Corn Flours Obtained by Traditional Nixtamalization Process
Authors: Rojas‐Molina I. , Gutiérrez E. , Rojas A. , Cortés‐Álvarez M. , Campos‐Solís L. , Hernández‐Urbiola M. , Arjona J. L. , Cornejo A. , Rodríguez‐García M. E. 
Published: September 2009

ABSTRACTThis report shows the effect of temperature (72, 82, and 92°C) during the cooking stage and steeping time (0, 1, 3, 5, 7, 9, 11, 13, and 15 hr) on calcium and phosphorus contents in nixtamalized corn flours obtained by the traditional nixtamalization process (NCF). In addition, calcium and phosphorus contents in industrial nixtamalized corn flours were analyzed for comparative purposes. Atomic absorption spectroscopy and UV‐vis spectroscopy methods were used to study the calcium and phosphorus contents as well as the Ca2+/P ratio in NCF and industrial nixtamalized corn flours. Additionally, deposition and identification of calcium compounds in the nixtamalized corn pericarp were analyzed by low‐vacuum scanning electron microscopy, energy dispersive spectrometry, and X‐ray diffraction techniques. Dry matter loss in NCF is also reported. As the temperature increased, Ca2+ content was enhanced, while the phosphorus content decreased with statistical differences (P ≤ 0.05) between thermal treatments. Ca2+ content in industrial nixtamalized corn flours was significantly lower (P ≤ 0.05) than that of NCF. On the other hand, no statistical differences (P ≤ 0.05) were found between phosphorus content in commercial nixtamalized corn flours and NCF. Calcium compounds, identified as calcite, were detected in corn pericarp. Statistical differences (P ≤ 0.05) were observed in phosphorous content in NCF obtained at different cooking temperatures. In addition, a decrease in phosphorus levels significantly correlated with the steeping time at 92°C (r = –0.91). At 72, 82, and 92°C, the average Ca2+/P ratio in NCF was 0.45 ± 0.03, 0.61 ± 0.05, and 0.82 ± 0.05, respectively, indicating a correlation between this parameter and the cooking temperature. However, no correlation was found between the Ca2+/P ratio and the steeping time. This behavior is attributed to calcium attached to corn kernel. In commercial nixtamalized corn flours, the Ca2+/P ratio was significantly lower (P ≤ 0.05) than that of NCF. There was a significant correlation (P ≤ 0.01) between dry matter loss and steeping time (r = 0.99) in NCF, this fact influenced the Ca2+/P ratio due to the calcium attached to pericarp. At 82 and 92°C, maximum values of Ca2+/P ratio were detected in NCF at 7 hr of steeping time and at 9 hr at 72°C. These results can be used with industrial purposes to assess a maximum calcium‐to‐phosphorus ratio, and at the same time, to avoid the loss of pericarp to increase the functional properties of NCF.
The ins and outs of extracellular matrix assembly
Authors: Kadler Karl E. 
Published: September 2009

Introduction  To a rough approximation, the adult human comprises 2–5 kg of cells. The remaining mass originates from the extracellular matrix (ECM). The ECM is highly organized, which is surprising considering the paucity of cells and the fact that the ECM comprises some of the largest and most insoluble macromolecules encoded by the genome. The high level of supramolecular order of the ECM is particularly evident in tendon in which millimetre‐long collagen fibrils lie parallel to each other and to the tendon‐long axis (Canty & Kadler 2002). The work in our laboratory is focused on understanding the molecular and cellular basis of collagen fibrillogenesis. The work is directly relevant to understanding the secretion and assembly of large proteins, tissue homeostasis and embryonic development, as well as understanding the aetiology of heritable and acquired diseases of connective tissue including fibrosis.Materials and methods  A multidisciplinary approach is being used including protein biochemistry, recombinant protein expression, immunofluorescence, immunoEM and serial section reconstruction from electron micrographs.Results  Using pulse‐chase in organ cultures of embryonic chick tendon we show that approximately 50% of newly synthesized type‐I procollagen is secreted to the ECM where it is cleaved to type‐I collagen, and approximately 50% of the procollagen is cleaved to collagen inside the cells. ImmunoEM shows collagen in specialized secretory vesicles, which bud from the trans‐face of the Golgi apparatus. Serial section reconstruction of E13 chick metatarsal tendon and E15.5 mouse tail tendon shows cross‐striated nascent collagen fibrils, which are approximately 1 µm in length and identical to collagen early collagen fibrils (Graham et al. 2000), enclosed within tube‐like secretory vesicles. The nascent fibrils are secreted via nozzles (plasma membrane protrusions) into tunnel‐shaped spaces between the cells. Bone morphogenetic protein‐1 (ProBMP‐1) is cleaved to active BMP‐1 in the TGN by dibasic convertases (Graham et al. 2000) (e.g. furin) and thereby initiates the assembly of collagen fibrils. Further studies have identified the minimal structure of procollagen C‐proteinase activity of BMP‐1 (Leighton & Kadler 2003).Discussion  In vitro studies in the 1980s established that collagen fibrillogenesis resembles a crystallization process, in that it proceeds by distinct nucleation and propagation phases. However, there was no obvious mechanism for how the two phases occurred separately in vivo. Our recent studies show that the nucleation phase occurs in specialized secretory vesicles. The early fibrils are deposited in the ECM via nozzles which are long protrusions of the plasma membranes. The propagation phase for fibril assembly occurs in the ECM. Our studies have direct relevance to the assembly of other matrix polymers, e.g. fibrillin and type‐VI collagen, as well as understanding the molecular basis of ECM assembly in diseases such as fibrosis and wound healing.
Decorin in renal inflammation and fibrosis – more than an inhibitor of TGF‐β
Authors: Schaefer Liliana 
Published: September 2009

Introduction  Decorin, a small leucine‐rich proteoglycan, participates in extracellular matrix assembly and influences cell behaviour by interacting with signalling membrane receptors and TGF‐β. Treatment with decorin has been shown to have beneficial effects in an acute model of mesangioproliferative glomerulonephritis due to interaction with TGF‐β. The underlying mechanisms, however, remain unclear because upon complex formation with TGF‐β, the cytokine's activity may become increased, decreased or not influenced at all. Hence, the objectives of the present study were twofold: firstly, to provide evidence that decorin influences the course and final outcome of renal inflammation and secondly, to find anti‐fibrotic mechanisms of decorin both related and unrelated to the regulation of TGF‐β activity.Results  Based on our studies in human diabetic nephropathy, we postulate two regulatory mechanisms by which decorin modulates TGF‐β‐mediated fibrosis: (1) increased quantities of glomerular decorin are synthesized and form complexes with TGF‐β, which then are removed via glomerular capillaries or the urinary tract, and (2) in the presence of type‐I collagen, decorin is able to sequester TGF‐β in the extracellular matrix, thereby withdrawing the cytokine from its cell‐surface receptors. Furthermore, we have compared the evolution of tubulointerstitial fibrosis in wild‐type (WT) and decorin–/– mice in a model of unilateral ureteral obstruction. Without obstruction, kidneys from decorin–/– mice did not differ in any aspect from their WT counterparts. However, already 12 h after obstruction, decorin–/– animals showed lower levels of p27KIP1 and soon thereafter a more pronounced up‐regulation and activation of initiator and effector caspases, followed by enhanced apoptosis of tubular epithelial cells. At later stages, a higher increase of TGF‐β1 became apparent. After 7 days, there was a 15‐fold transient up‐regulation of the related proteoglycan biglycan, which was mainly caused by the appearance of biglycan‐expressing mononuclear cells. Other small proteoglycans showed no similar response. Owing to enhanced degradation of type‐I collagen and increased tubular epithelial cell apoptosis, end‐stage kidneys from decorin–/– animals were more atrophic than WT kidneys.Conclusion  These data suggest that decorin exerts beneficial effects on renal inflammation, primarily by influencing the expression of a key cyclin‐dependent kinase inhibitor, thereby limiting the degree of apoptosis and tubular atrophy. In later stages, anti‐fibrotic effects of decorin are based on the regulation of TGF‐β1 expression, mononuclear cell infiltration and collagen turnover.
Matrix‐metabolizing enzymes as prime targets of redox regulation by nitric oxide
Authors: Pfeilschifter Josef , Akool El Sayed , Eberhardt Wolfgang 
Published: September 2009

Introduction  Dysregulation of extracellular matrix (ECM) turnover is an important feature of many inflammatory processes in the kidney. Rat mesangial cells (MCs) express high levels of inducible nitric oxide synthase (iNOS) and matrix metalloproteinase‐9 (MMP‐9) in response to interleukin‐1β (IL‐1β) (Pfeilschifter & Schwarzenbach 1990; Eberhardt et al. 2000a). The aim of our studies was to elucidate the mechanisms of NO‐dependent modulation of MMP‐9 expression.Methods  The expression level of MMP‐9 was detected by zymography and by Northern blot analysis, respectively. The influence of NO on mRNA stability was measured by use of actinomycin‐D and by Luciferase reporter gene assays using heterologous MMP‐9 reporter gene constructs. The effects of NO on MMP‐9 transcripts were monitored by in vitro degradation assays and RNA‐binding activity determined by electrophoretic mobility shift assays (EMSA).Results  MMP‐9 (gelatinase‐B) is a metalloproteinase that is synthesized and secreted in high levels by the glomerular MCs upon treatment with the proinflammatory cytokine IL‐1β mainly via an increase in MMP‐9 transcription (Eberhardt et al. 2000a). The increase in MMP‐9 expression by cytokines is partially due to generation of superoxide and involves the activation of different MAPK pathways (Eberhardt et al. 2000b). Furthermore, we demonstrate that NO substantially inhibits the cytokine‐induced expression of MMP‐9 without affecting MMP‐9 enzyme activity (Eberhardt et al. 2000a). By using actinomycin‐D, we found that NO reduces the half‐life of MMP‐9 mRNA (Akool et al. 2003). The reduction of mRNA stability is attributable to the 3′‐untranslated region of MMP‐9 since introduction of this region confered a negative NO responsiveness to an otherwise nonresponding heterologous MMP‐9 reporter luciferase gene (Akool et al. 2003). By EMSA, we found that cytoplasmic fractions display the consitutive RNA binding of complexes containing the ELAV‐like protein HuR (HuA). Moreover, the RNA binding to three putative AU‐rich elements (AREs) is strongly attenuated by different NO donors (Akool et al. 2003). Correspondingly, the decay of MMP‐9 transcripts was accelerated by cytoplasmic extracts from NO‐treated MCs as shown by in vitro degradation assay (Akool et al. 2003).Conclusion  NO negatively regulates cytokine‐induced MMP‐9 expression by a post‐transcriptional mechanism which involves inhibition of the mRNA stabilizing ELAV‐like protein HuR.
Emodin ameliorates glucose‐induced fibronectin synthesis in human peritoneal mesothelial cells by inhibiting PKC‐α activation
Authors: Yung Susan , Leung Jack , Tsang Ryan , Liu Zhi Hong , Li Lei Shi , Chan Tak Mao 
Published: September 2009

Introduction Peritoneal dialysis (PD) is recognized as an effective treatment for patients with end‐stage renal failure. Conventional PD solutions are unphysiological, as they contain bio‐incompatible concentrations of glucose to provide the osmotic drive (Popovichet al. 1978) Thus, with increasing duration on PD, the peritoneum undergoes progressive structural and functional deterioration. Diabetiform alterations of the peritoneum, for example, the reduplication of the basement membrane, and increased matrix accumulation and deposition within the submesothelium are commonly observed in PD patients. These changes are mediated in part through activation of PKC and induction of TGF‐β1 (Haet al. 2001). Emodin (3‐methyl‐1,6,8 trihydroxyanthraquinone) has previously been demonstrated to reduce cell proliferation and fibronectin synthesis in cultured mesangial cells (Kuoet al. 2001;Yaoet al. 1994). How emodin modulates glucose‐induced fibronectin synthesis in human peritoneal mesothelial cells (HPMCs) has not been elucidated and thus constitutes the aim of this study.Materials and methods Confluent growth‐arrested HPMCs were cultured under physiological (5 mm) or elevated (30 mm) d‐glucose concentrations in the presence or absence of emodin (20 µg/ml) for periods up to 72 h. PKC‐α activation in HPMCs cultured under control and experimental conditions was determined by Western blot analysis of cytosolic and cell membrane extracts. Synthesis of fibronectin and TGF‐β1 was investigated by a combination of ELISAs, immunohistochemistry and Western blot analysis. Mannitol was used as the hexose control.Results Exposure of HPMCs to 30 mm d‐glucose resulted in the activation of PKC‐α commencing 12 h after stimulation, as demonstrated by the translocation of PKC‐α from the cytosol to the cell membrane. Maximum induction of PKC‐α was observed 48 h after stimulation and increased 1.4‐fold and 3.7‐fold in the cytosolic and membrane fractions, respectively, compared to 5 mm d‐glucose. Activation of PKC‐α was accompanied by the induction of TGF‐β1 secretion in a time‐dependent manner (3.72 ± 0.29 and 4.30 ± 0.50 pg/µg cellular protein at 24 h and 48 h, respectively, for 30 mm d‐glucose compared to 2.13 ± 0.23 and 2.65 ± 0.32 pg/µg cellular protein at 24 h and 48 h, respectively, for 5 mm d‐glucose,P < 0.001 at both time points) and increased fibronectin synthesis. Whilst emodin had no effect on constitutive PKC‐α, TGF‐β1 or fibronectin synthesis, emodin abrogated elevated glucose stimulation of PKC‐α, and decreased TGF‐β1 secretion and fibronectin synthesis to basal levels.Discussion Our findings demonstrate that emodin can ameliorate the undesirable effects of concentrated glucose on HPMCs through the suppression of PKC‐α activation. This study suggests that emodin may have therapeutic potential in the prevention or treatment of glucose‐induced structural and functional abnormalities in the peritoneal membrane.
TGF‐β promotes the formation of pyridinoline cross‐links in fibrosis via the induction of LH2 expression
Authors: Slot Annemarie J. Van Der , Zuurmond Anne‐Marie , Abraham David J. , Bank Ruud A. 
Published: September 2009

Introduction  The hallmark of fibrosis is an excessive accumulation of collagen, a process in which TGF‐β plays an important role. The deposited collagen shows an increase in pyridinoline cross‐links, due to overhydroxylation of lysine residues within the telopeptides. As we have found that the enzyme responsible for the hydroxylation of the telepeptide lysine residues is lysyl hydroxylase‐2 (LH2), it was examined whether LH2 is increased in fibrotic lesions. TGF‐β is a key mediator in fibrosis, and therefore its effect on the formation of pyridinolines was examined.Material and methods  Using real‐time PCR, LH2 mRNA expression was measured in fibroblasts cultured from the fibrotic skin of systemic sclerosis (SSc) patients. Furthermore, the amount of pyridinoline cross‐links was analysed in the matrix deposited by fibroblasts stimulated with TGF‐β.Results  Elevated LH2 mRNA expression levels were found in SSc fibroblasts, which result in increased amounts of pyridinoline cross‐links. Furthermore, increased pyridinoline levels were found in collagen deposited by fibroblasts stimulated with TGF‐β, which was a consequence of increased LH2 mRNA levels.Conclusion  These data demonstrate for the first time that during fibrotic processes, TGF‐β plays a key role in the formation of pyridinoline cross‐links via the induction of LH2 expression.