bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sensate scaffolds can reliably detect joint loading
Authors: Bliss C. L. , Szivek J. A. , Tellis B. C. , Margolis D. S. , Schnepp A. B. , Ruth J. T. 
Published: August 2006

AbstractTreatment of cartilage defects is essential to the prevention of osteoarthritis. Scaffold‐based cartilage tissue engineering shows promise as a viable technique to treat focal defects. Added functionality can be achieved by incorporating strain gauges into scaffolds, thereby providing a real‐time diagnostic measurement of joint loading. Strain‐gauged scaffolds were placed into the medial femoral condyles of 14 adult canine knees and benchtop tested. Loads between 75 and 130 N were applied to the stifle joints at 30°, 50°, and 70° of flexion. Strain‐gauged scaffolds were able to reliably assess joint loading at all applied flexion angles and loads. Pressure sensitive films were used to determine joint surface pressures during loading and to assess the effect of scaffold placement on joint pressures. A comparison of peak pressures in control knees and joints with implanted scaffolds, as well as a comparison of pressures before and after scaffold placement, showed that strain‐gauged scaffold implantation did not significantly alter joint pressures. Future studies could possibly use strain‐gauged scaffolds to clinically establish normal joint loads and to determine loads that are damaging to both healthy and tissue‐engineered cartilage. Strain‐gauged scaffolds may significantly aid the development of a functional engineered cartilage tissue substitute as well as provide insight into the native environment of cartilage. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2006
Asymmetrical regulation of scavenger receptor class B type I by apical and basolateral stimuli using Caco‐2 cells
Authors: Peretti N. , Delvin E. , Sinnett D. , Marcil V. , Garofalo C. , Levy E. 
Published: August 2006

AbstractCholesterol uptake and the mechanisms that regulate cholesterol translocation from the intestinal lumen into enterocytes remain for the most part unclear. Since scavenger receptor class B type I (SR‐BI) has been suggested to play a role in cholesterol absorption, we investigated cellular SR‐BI modulation by various potential effectors administered in both apical and basolateral sides of Caco‐2 cells. With differentiation, Caco‐2 cells increased SR‐BI protein expression. Western blot analysis showed the ability of cholesterol and oxysterols in both cell compartments to reduce SR‐BI protein expression. Among the n‐3, n‐6, and n‐9 fatty acid families, only eicosapentaenoic acid was able to lower SR‐BI protein expression on both sides, whereas apical α‐linolenic acid decreased SR‐BI abundance and basolateral arachidonic acid (AA) raised it. Epidermal growth factor and growth hormone, either in the apical or basolateral medium, diminished SR‐BI cellular content, while insulin displayed the same effect only on the basolateral side. In the presence of proinflammatory agents (LPS, TNF‐α, IFN‐γ), Caco‐2 cells exhibited differential behavior. SR‐BI was downregulated by lipopolysaccharide on both sides. Finally, WY‐14643 fibrate diminished SR‐BI protein expression when it was added to the apical medium. Biotinylation studies in response to selected stimuli revealed that regulatory modifications in SR‐BI protein expression occurred for the most part at the apical cell surface irrespective of the effector location. Our data indicate that various effectors supplied to the apical and basolateral compartments may impact on SR‐BI at the apical membrane, thus suggesting potential regulation of intestinal cholesterol absorption and distribution in various intracellular pools. J. Cell. Biochem. 100: 421–433, 2007. © 2006 Wiley‐Liss, Inc.
Reconstitution of Runx2/Cbfa1‐null cells identifies a requirement for BMP2 signaling through a Runx2 functional domain during osteoblast differentiation
Authors: Bae Jong‐Sup , Gutierrez Soraya , Narla Radhika , Pratap Jitesh , Devados Rajitha , van Wijnen Andre J. , Stein Janet L. , Stein Gary S. , Lian Jane B. , Javed Amjad 
Published: August 2006

AbstractThe Runx2/Cbfa1 transcription factor is a scaffolding protein that promotes osteoblast differentiation; however, the specific Runx2‐functional domains required for induction of the osteogenic lineage remain to be identified. We approached this question using a TERT‐immortalized cell line derived from calvaria of Runx2‐null mice by reconstituting the osteogenic activity with wild‐type and deletion mutants of Runx2. The presence or absence of osteogenic media (β‐glycerol phosphate and ascorbic acid) and/or with BMP2 did not stimulate osteoblastic gene expression in the Runx2‐null cells. However, cells infected with wild‐type Runx2 adenovirus showed a robust temporal increase in the expression of osteoblast marker genes and were competent to respond to BMP2. Early markers (i.e., collagen type‐1, alkaline phosphatase) were induced (four‐ to eightfold) at Days 4 and 8 of culture. Genes representing mature osteoblasts (e.g., Runx2, osteopontin, bone sialoprotein, osteocalcin) were temporally expressed and induced from 18‐ to 36‐fold at Days 8 and 12. Interestingly, TGFβ and Vitamin D‐mediated transcription of osteoblast genes (except for osteopontin) required the presence of Runx2. Runx2 lacking the C‐terminal 96 amino acids (Runx2 Δ432) showed a pattern of gene expression similar to wild‐type protein, demonstrating the Groucho interaction and part of the activation domain are dispensable for Runx2 osteogenic activity. Upon further deletion of the Runx2 C‐terminus containing the nuclear matrix targeting signal and Smad‐interacting domain (Δ391), we find none of the osteoblast markers are expressed. Therefore, the Runx2 391‐432 domain is essential for execution of the BMP2 osteogenic signal. J. Cell. Biochem. 100: 434–449, 2007. © 2006 Wiley‐Liss, Inc.
DNA damage‐induced RPA focalization is independent of γ‐H2AX and RPA hyper‐phosphorylation
Authors: Liu Jen‐Sing , Kuo Shu‐Ru , Melendy Thomas 
Published: August 2006

AbstractReplication protein A (RPA) is the major eukaryotic single stranded DNA binding protein that plays a central role in DNA replication, repair and recombination. Like many DNA repair proteins RPA is heavily phosphorylated (specifically on its 32 kDa subunit) in response to DNA damage. Phosphorylation of many repair proteins has been shown to be important for their recruitment to DNA damage‐induced intra‐nuclear foci. Further, phosphorylation of H2AX (γ‐H2AX) has been shown to be important for either the recruitment or stable retention of DNA repair proteins to these intra‐nuclear foci. We address here the relationship between DNA damage‐induced hyper‐phosphorylation of RPA and its intra‐nuclear focalization, and whether γ‐H2AX is required for RPA's presence at these foci. Using GFP‐conjugated RPA, we demonstrate the formation of extraction‐resistant RPA foci induced by DNA damage or stalled replication forks. The strong DNA damage‐induced RPA foci appear after phosphorylated histone H2AX and Chk1, but earlier than the appearance of hyper‐phosphorylated RPA. We demonstrate that while the functions of phosphoinositol‐3‐kinase‐related protein kinases are essential for DNA damage‐induced H2AX phosphorylation and RPA hyper‐phosphorylation, they are dispensable for the induction of extraction‐resistant RPA and RPA foci. Furthermore, in mouse cells genetically devoid of H2AX, DNA damage‐induced extraction‐resistant RPA appears with the same kinetics as in normal mouse cells. These results demonstrate that neither RPA hyper‐phosphorylation nor H2AX are required for the formation in RPA intra‐nuclear foci in response to DNA damage/replicational stress and are consistent with a role for RPA as a DNA damage sensor involved in the initial recognition of damaged DNA or blocked replication forks. J. Cell. Biochem. 99: 1452–1462, 2006. © 2006 Wiley‐Liss, Inc.
The cellular control of DNA double‐strand breaks
Authors: Scott Shaun P. , Pandita Tej K. 
Published: August 2006

AbstractDNA double‐strand breaks (DSBs) are the most hazardous lesions arising in the genome of eukaryotic organisms, and yet occur normally during DNA replication, meiosis, and immune system development. The efficient repair of DSBs is crucial in maintaining genomic integrity, cellular viability, and the prevention of tumorigenesis. As a consequence, eukaryotic cells have evolved efficient mechanisms that sense and respond to DSBs and ultimately repair the break. The swiftness of the DNA DSB response has paved to the identification of sensors and transducers which allowed to generate a hierarchical signaling paradigm depicting the transduction of the damage signal to numerous downstream effectors (Fig. 1). The function of such effectors involve posttranslational modifications through phosphorylation, acetylation, and methylation of the substrates. This review will address the control of DSBs in damaged eukaryotic cells, the physiological processes that require the introduction of a DSB into the genome, and the maintenance of DSBs in non‐damaged cells. J. Cell. Biochem. 99: 1463–1475, 2006. © 2006 Wiley‐Liss, Inc.
Utilizing SENSE to reduce scan duration in high‐resolution contrast‐enhanced renal MR angiography
Authors: Wilson Gregory J. , Eubank William B. , Vasbinder G. Boudewijn C. , Kessels Alfons G.H. , Hoogeveen Romhild M. , Muthupillai Raja , Maki Jeffrey H. 
Published: August 2006

AbstractPurposeTo evaluate the use of sensitivity encoding (SENSE) to reduce scan time and decrease detrimental artifacts arising from motion and bolus profile effects during contrast‐enhanced MR angiography (CE‐MRA) of the renal arteries (RAs).Materials and MethodsA direct comparison of conventional and SENSE (acceleration factor 2) CE‐MRA protocols was performed on 20 patients. Each patient underwent both scans. Both protocols achieved the same resolution, but the SENSE protocol was 50% faster and utilized a faster injection than the conventional scan. Three radiologists graded the images for image quality, artifact levels, and reader confidence.ResultsWhile the signal‐to‐noise ratio (SNR) decreased (26 ± 5 vs. 30 ± 10; P = 0.04) with the SENSE protocol, the image‐quality scores for four identified segments of the RAs increased or were unchanged. The largest improvements in image quality occurred in the more distal segments of the RAs. Parenchymal ringing (P = 0.005) and RA blurring (P = 0.006) were significantly reduced, and there was a trend toward improvement of RA ringing despite the increased injection rate.ConclusionThe faster SENSE scan maintained nearly the same SNR (due to faster injection of Gd‐chelate), reduced artifact levels, and improved image quality ratings for the distal renal vessels. J. Magn. Reson. Imaging 2006. © 2006 Wiley‐Liss, Inc.
Measurement of single kidney function using dynamic contrast‐enhanced MRI: Comparison of two models in human subjects
Authors: Buckley David L. , Shurrab Ala'a E. , Cheung Ching M. , Jones Andrew P. , Mamtora Hari , Kalra Philip A. 
Published: August 2006

AbstractPurposeTo compare two methods for assessing the single kidney glomerular filtration rate (SK‐GFR) in humans using dynamic contrast‐enhanced (DCE)‐MRI.Materials and MethodsImages were acquired from 39 separate MR studies of patients with atherosclerotic renovascular disease (ARVD). Data from the kidneys and descending aorta were analyzed using both a Rutland‐Patlak plot and a compartmental model. MR estimates of the SK‐GFR were compared with standard radioisotope measures in a total of 75 kidneys.ResultsEstimates of renal function using both techniques correlated well with radioisotope‐assessed SK‐GFR (Spearman's ρ = 0.81, Rutland‐Patlak; ρ = 0.71, compartmental model). The Rutland‐Patlak approach provided a near one‐to‐one correspondence, while the compartmental method tended to overestimate SK‐GFR. However, the compartmental model fits to the experimental data were significantly better than those obtained using the Rutland‐Patlak approach.ConclusionDCE‐MRI of the kidneys provides data that correlate well with reference measures of SK‐GFR. However, further work, including image registration, is needed to isolate measurement of glomerular filtration to the level of the renal cortex. J. Magn. Reson. Imaging 2006. © 2006 Wiley‐Liss, Inc.
Association of genetic polymorphism of low‐density lipoprotein receptor with chronic viral hepatitis C infection in Han Chinese
Authors: Li Han , Liu Zhengwen , Han Qunying , Li Yan , Chen Jinghong 
Published: August 2006

AbstractTo study the association between the Ava II polymorphism at the low‐density lipoprotein receptor (LDL‐R) gene exon 13 locus and chronic hepatitis C virus (HCV) infection in the Han Chinese, 84 chronic HCV‐infected patients without anti‐viral treatment, and 72 healthy blood donors were studied. Polymerase chain reaction combined with restriction fragment length polymorphism (PCR‐RFLP) was used to detect the Ava II polymorphism at the LDL‐R gene exon 13 locus. The comparisons of genotype distribution and allele frequency between chronic HCV‐infected patients and healthy controls showed statistically significant differences (P = 0.045 and P = 0.036, respectively). Additionally, the minor allele frequency (MAF) C in the healthy controls was higher than that in the chronic HCV‐infected patients group. There was no significant difference (P = 0.130) when the genotype distribution was compared between chronic HCV‐infected patients with HCV viremia and those without HCV viremia. However, the comparisons of allele frequency between the two groups showed a statistically significant difference (P = 0.047), and the MAF C in HCV RNA negative group was significantly higher than that in HCV RNA positive group. There were no significant differences in genotype distribution and allele frequency of the Ava II restriction site at the LDL‐R gene exon 13 locus between patients with chronic HCV infection and those with HCV‐associated cirrhosis as well as between patients with normal serum alanine aminotransferase (ALT) and those with abnormal ALT levels. These results suggest that the Han Chinese have Ava II polymorphism at the LDL‐R gene exon 13 locus. The Ava II polymorphism at the LDL‐R gene exon 13 locus showed a statistically significant difference between chronic HCV‐infected patients and healthy controls, indicating a significant contribution of the Ava II polymorphism in susceptibility to HCV infection in these patients. The MAF C in HCV RNA negative group was higher than that in HCV RNA positive group, suggesting that the Ava II polymorphism might also be associated with viremia in patients with HCV infection. J. Med. Virol. 78:1289–1295, 2006. © 2006 Wiley‐Liss, Inc.
The prevalence of human papillomavirus genotypes in penile cancers from northern Thailand
Authors: Senba Masachika , Kumatori Atsushi , Fujita Shuichi , Jutavijittum Prapan , Yousukh Amnat , Moriuchi Toshiyuki , Nakamura Tsuyoshi , Toriyama Kan 
Published: August 2006

AbstractThe highest frequency of penile cancer occurs in Asia, Africa, and Latin America, and there have been a few reports concerning the association of penile cancer with human papillomavirus (HPV) infection in these areas. The objective of this study was to determine the relation between penile cancer and the prevalence of HPV genotypes in northern Thailand. Eighty‐eight specimens of penile tissue (65 malignant, 1 pre‐malignant, and 22 benign cases) were examined to determine the association of HPV infection. An in situ hybridization (ISH) method was used to detect and localize HPV‐DNA. Sensitive HPV polymerase chain reaction (PCR) procedure was used for detection of HPV‐DNA, and DNA sequencing was used to identify the HPV genotype. HPV‐DNA was detected in 53.8% and 81.5% of cases of penile cancer, using ISH and PCR, respectively. The high‐risk HPV‐16, most commonly associated with penile cancer in previous reports, was found in only one case in this study. The most prevalent genotype was the high‐risk HPV‐18, found in 55.4% of the cases (32.3% single and 23.1% multiple infection) followed by the low‐risk HPV‐6, found in 43.1% of the cases (24.6% single and 18.5% multiple infection). In this study, penile cancer was found to be highly correlated with HPV‐DNA. Specifically, infection with both the low‐risk HPV‐6 and the high‐risk HPV‐18 is the characteristic prevalence of HPV genotypes in penile cancer in this area. J. Med. Virol. 78:1341–1346, 2006. © 2006 Wiley‐Liss, Inc.
Batten disease (JNCL) is linked to disturbances in mitochondrial, cytoskeletal, and synaptic compartments
Authors: Luiro Kaisu , Kopra Outi , Blom Tomas , Gentile Massimiliano , Mitchison Hannah M. , Hovatta Iiris , Törnquist Kid , Jalanko Anu 
Published: August 2006

AbstractIntracellular pathways leading to neuronal degeneration are poorly understood in the juvenile neuronal ceroid lipofuscinosis (JNCL, Batten disease), caused by mutations in the CLN3 gene. To elucidate the early pathology, we carried out comparative global transcript profiling of the embryonic, primary cultures of the Cln3−/− mouse neurons. Statistical and functional analyses delineated three major cellular pathways or compartments affected: mitochondrial glucose metabolism, cytoskeleton, and synaptosome. Further functional studies showed a slight mitochondrial dysfunction and abnormalities in the microtubule cytoskeleton plus‐end components. Synaptic dysfunction was also indicated by the pathway analysis, and by the gross upregulation of the G protein beta 1 subunit, known to regulate synaptic transmission via the voltage‐gated calcium channels. Intracellular calcium imaging showed a delay in the recovery from depolarization in the Cln3−/− neurons, when the N‐type Ca2+ channels had been blocked. The data suggests a link between the mitochondrial dysfunction and cytoskeleton‐mediated presynaptic inhibition, thus providing a foundation for further investigation of the disease mechanism underlying JNCL disease. © 2006 Wiley‐Liss, Inc.
Apolipoprotein E exerts selective and differential control over vitamin E concentrations in different areas of mammalian brain
Authors: Vatassery Govind T. , Lam Cornelius , Smith W. Ed , Quach Hung T. 
Published: August 2006

AbstractApolipoprotein E (apoE) is known to be a risk factor for the incidence of Alzheimer's disease (AD). In addition, vitamin E has been reported to have a role in the treatment of AD. We examined the potential interrelationship between vitamin E and apoE in brain. As the first step, we determined the concentrations of α‐tocopherol in selected brain regions of apoE‐deficient mice at different ages. The mice were fed normal rodent chow. All regions of the brain in apoE‐deficient mice contained less α‐tocopherol than control samples at 2.5 months of age, the initial time of study. This trend continued for 9.5 months for most regions except the spinal cord and cerebellum. Tocopherol levels in these latter regions of apoE‐deficient animals increased to control levels during the study. Serum α‐tocopherol and cholesterol levels were high in the apoE‐deficient animals; however, the CNS cholesterol levels were the same in apoE‐deficient and control mice. This suggests that 1) the decline in brain α‐tocopherol in apoE deficiency is not due to overall alterations in lipid metabolism; and 2) the processing of α‐tocopherol in brain follows a separate pathway than that of cholesterol. Subcellular concentrations of α‐tocopherol were unaltered by apoE deficiency indicating that intracellular handling of tocopherol is not affected by apoE. ApoE may be an important protein controlling vitamin E levels in specific brain regions. Further understanding of the interactions between apoE and vitamin E could be important in the appropriate use of vitamin E in AD. © 2006 Wiley‐Liss, Inc.
Novel roles for metallothionein‐I + II (MT‐I + II) in defense responses, neurogenesis, and tissue restoration after traumatic brain injury: Insights from global gene expression profiling in wild‐type and MT‐I + II knockout mice
Authors: Penkowa Milena , Cáceres Mario , Borup Rehannah , Nielsen Finn Cilius , Poulsen Christian Bjørn , Quintana Albert , Molinero Amalia , Carrasco Javier , Florit Sergi , Giralt Mercedes , Hidalgo Juan 
Published: August 2006

AbstractTraumatic injury to the brain is one of the leading causes of injury‐related death or disability, especially among young people. Inflammatory processes and oxidative stress likely underlie much of the damage elicited by injury, but the full repertoire of responses involved is not well known. A genomic approach, such as the use of microarrays, provides much insight in this regard, especially if combined with the use of gene‐targeted animals. We report here the results of one of these studies comparing wild‐type and metallothionein‐I + II knockout mice subjected to a cryolesion of the somatosensorial cortex and killed at 0, 1, 4, 8, and 16 days postlesion (dpl) using Affymetrix genechips/oligonucleotide arrays interrogating ∼10,000 different murine genes (MG_U74Av2). Hierarchical clustering analysis of these genes readily shows an orderly pattern of gene responses at specific times consistent with the processes involved in the initial tissue injury and later regeneration of the parenchyma, as well as a prominent effect of MT‐I + II deficiency. The results thoroughly confirmed the importance of the antioxidant proteins MT‐I + II in the response of the brain to injury and opened new avenues that were confirmed by immunohistochemistry. Data in KO, MT‐I‐overexpressing, and MT‐II‐injected mice strongly suggest a role of these proteins in postlesional activation of neural stem cells. © 2006 Wiley‐Liss, Inc.
The meteorological data of William Hutchinson and a Liverpool air pressure time series spanning 1768–1999
Authors: Woodworth Philip L. 
Published: August 2006

AbstractThis paper discusses some of the meteorological measurements made at Liverpool by Captain William Hutchinson in the second half of the eighteenth century. It gives an overview of the various data sets, most of which are now in computer‐accessible form, and provides assessments of their quality, the aim being to gain an overall impression of how good an observer Hutchinson was. His air pressure data have been studied in detail, through comparisons with information from other UK stations, and via investigation of the sea‐level response to air pressure changes as observed in his tidal measurements. A first attempt has been made to construct a Liverpool air pressure time series spanning 1768–1999, by means of the combination of Hutchinson's data with later information from the Liverpool docks and Bidston Observatory. Copyright © 2006 Royal Meteorological Society