bluuebunny/crossref_metadata_2025_split huggingface dataset:
Synthesizing Citizenship in Modern China1
Authors: Culp Robert 
Published: October 2007

AbstractThis article reviews the recent scholarship on citizenship in early twentieth‐century China and presents a conceptual framework for analyzing citizenship, there and elsewhere, as a complex formation of ideas and practices. The article asks why citizenship became so important in late Qing and early Republican China and why Euro‐American scholars have been so attentive to it during the last two decades. It then draws on the rich historical literature to characterize four distinct dimensions of modern Chinese citizenship. In discussing national identity, political participation and civil rights, cultural citizenship, and social membership, the author reflects on possible axes of comparison between Chinese and Euro‐American approaches to citizenship. Finally, the article argues that these four aspects can be viewed as part of a composite whole that identified Chinese citizenship with active participation in concrete tasks to contribute to national welfare.
British Exploration in the Nineteenth Century: A Historiographical Survey
Authors: Kennedy Dane 
Published: October 2007

AbstractThis article examines the historiography on nineteenth‐century British exploration, tracing major themes in the scholarship on the subject. It credits the work of Edward Said, Mary Louise Pratt, and Paul Carter as the main inspiration for the resurgence of academic interest in the history and literature of travel and exploration, though it also indicates that there are important limitations to the approach they pioneered. The article then traces two key themes of recent work on exploration. The first theme concerns the institutional, social, and intellectual forces in Britain that inspired the exploration of other lands and oversaw its operations. The second theme concerns the cultural encounter between explorers and indigenous peoples, which ranged in its effects from the psychic to the political realm.
Connective tissue growth factor increases matrix metalloproteinase‐2 and suppresses tissue inhibitor of matrix metalloproteinase‐2 production by cultured renal interstitial fibroblasts
Authors: Yang Min , Huang Haichang , Li Jingzi , Huang Wen , Wang Haiyan 
Published: October 2007

ABSTRACTThe involvement of gelatinase (matrix metalloproteinase‐2 [MMP‐2] and MMP‐9) in the matrix remodeling and development of tubulointerstitial fibrosis has been studied recently, but relatively little is known about the regulators and the mechanisms controlling the activation and expression of gelatinase in renal fibroblasts. In these studies, the production and underlying signaling pathway for gelatinase by exogenous connective tissue growth factor (CTGF) treatment were investigated. Here, we show that CTGF acts as a potent promoter of the activation and expression of MMP‐2, but not MMP‐9 in normal rat kidney fibroblasts cell line (NRK‐49F). We found that CTGF significantly increased the activity of MMP‐2, as well as MMP‐2 protein in conditioned medium and MMP‐2 mRNA levels in cells. In studies to address the mechanisms involved in the regulation of MMP‐2 activity, we found that the tissue inhibitor of matrix metalloproteinase‐2 (TIMP‐2), the inhibitor of MMP‐2, decreased significantly when cells were treated with CTGF. Further studies showed that extracellular signal‐regulated kinase (ERK) signaling is responsible for most of the CTGF‐induced MMP‐2 expression and TIMP‐2 suppression. When NRK‐49F fibroblasts were incubated with CTGF, activation of ERK1/2 signaling was observed. Suppression of ERK1/2 activation with nontoxic concentrations of PD98059, a specific inhibitor of ERK activation, was associated with a reduction of CTGF‐stimulated MMP‐2 activity and protein expression. In addition, the CTGF‐mediated reduction of TIMP‐2 activity and protein expression was prevented when ERK1/2 activation was inhibited by PD98059. These results provide evidence that CTGF augments activation of MMP‐2 through an effect on MMP‐2 protein expression and TIMP‐2 suppression, and that these effects are dependent on the activation of the ERK1/2 pathway.
Immobilized gradients of epidermal growth factor promote accelerated and directed keratinocyte migration
Authors: Stefonek Tracy Jane , Masters Kristyn S. 
Published: October 2007

ABSTRACTAcceleration of wound closure results not only in decreased patient suffering and cost of wound treatment, but may also minimize scarring and lead to formation of a more stable closed wound. Cell migration is a critical element in wound healing, and it is believed that the ability to control the migration direction of cells will lead to accelerated closure of wounds. Thus, we have synthesized surfaces that are covalently modified with gradients of epidermal growth factor (EGF), a key molecule in the native wound‐healing process, in order to create a platform that promotes directed cell migration. Standard photo‐patterning techniques used herein enabled precise control over the spatial location of tethered EGF and the fabrication and quantitative characterization of gradient patterns of different types and slopes. Under serum‐free conditions, human epidermal keratinocytes on immobilized EGF gradients preferentially migrated in the direction of higher EGF concentrations, and exhibited unidirectional migration speed and distance that was over five‐fold greater than that observed on control surfaces. Treatment of migrating cells with an inhibitor of the EGF receptor resulted in immediate cessation of migration, thus verifying that the observed migration trends were directly attributable to keratinocyte interactions with immobilized EGF.
Inhibition of keratinocyte migration by lipopolysaccharide
Authors: Loryman Chris , Mansbridge Jonathan 
Published: October 2007

ABSTRACTA critical process in cutaneous wound healing is reepithelialization by keratinocytes that closes the breach in the epidermis. Chronic wounds fail to reepithelialize despite the presence of activated and proliferative keratinocytes around the wound perimeter. This type of wound is generally colonized to a greater or lesser extent by bacteria. This study examines the possibility that bacterial products might directly inhibit keratinocyte migration. Using conventional scratch assays, we observed a dose‐dependent inhibition of keratinocyte migration by lipopolysaccharide (LPS) derived from either Pseudomonas aeruginosa or Escherichia coli. Although the P. aeruginosa preparation appeared to be slightly more inhibitory, both gave half‐maximal inhibition at 0.5–0.6 ng/mL. Migration of fibroblasts was not inhibited. The result could not be attributed to a cytotoxic effect of the LPS. LPS inhibition of migration was relieved by neutralizing antibodies to toll‐like receptors (TLR), 40% by anti‐TLR2 and 75% by anti‐TLR4. We conclude that keratinocyte migration is inhibited by bacterial products, detected through TLR4 and also through TLR2. Because chronic wounds always show some presence of bacteria, these findings provide a possible explanation for the lack of healing found in ulcers.
A neurokinin‐1 receptor antagonist that reduces intraabdominal adhesion formation increases peritoneal matrix metalloproteinase activity
Authors: Cohen Philip A. , Gower Adam C. , Stucchi Arthur F. , Leeman Susan E. , Becker James M. , Reed Karen L. 
Published: October 2007

ABSTRACTAdhesions remain a significant complication of abdominal surgery. There is a growing body of evidence suggesting that remodeling of peritoneal extracellular matrix by matrix metalloproteinases (MMPs) is involved in adhesion formation. We have shown that administration of a specific neurokinin‐1 receptor (NK‐1R) antagonist (CJ‐12,255, Pfizer) to rats within 5 hours of surgery reduces intraabdominal adhesion formation. Because substance P (SP), the primary NK‐1R ligand, is known to augment tissue fibrosis, the aim of this study was to determine the effects of NK‐1R antagonist administration on peritoneal MMP expression and activity 24 hours after surgery in a rat adhesion model. Following laparotomy, four ischemic buttons were created on the peritoneum of rats that received either an intraperitoneal NK‐1R antagonist or a vehicle at surgery. Adhesion formation was assessed 7 days later. Peritoneal fluid and tissue were collected at 24 hours to assess total MMP activity, as well as MMP‐2, MMP‐8, and MMP‐9 activity. Specific MMP and tissue inhibitors of MMP mRNAs were measured, and the effects of SP on MMP‐3 expression were determined in Met‐5A cells, a human peritoneal mesothelial cell line. NK‐1R antagonist administration reduced adhesion formation by 47% (p<0.05) at 7 days and significantly increased the total MMP activity in peritoneal fluid at 24 hours. There was an accompanying increase (p<0.05) in MMP‐8 and MMP‐9 mRNA expression and activity in peritoneal tissue and fluid, respectively. MMP‐3 mRNA was also increased in the 24‐hour peritoneal tissue, and exposure of Met‐5A cells to SP reduced MMP‐3 expression and activity. These data support a role for MMPs, specifically MMP‐3, MMP‐8, and MMP‐9, in intraabdominal adhesion formation and suggest that the NK‐1R antagonist may reduce adhesions, in part, by increasing MMP activity in the peritoneum by 24 hours after surgery.
Review: β‐Blockade in Chronic Dialysis Patients
Authors: Furgeson Seth B. , Chonchol Michel 
Published: October 2007

AbstractApproximately 50% of the mortality in chronic dialysis patients is due to cardiovascular diseases (CVD). Cardiomyopathy, coronary artery disease, and arrhythmia are all common conditions and predispose to sudden death, which accounts for 60% of all cardiac deaths in this population. Despite advances in dialysis therapy, the mortality from CVD remains substantially unchanged, partly due to the lack of evidence‐based strategies for improving the outcome of cardiac diseases in this population. Activation of the sympathetic adrenergic system is well documented in chronic dialysis patients and is likely involved in the pathogenesis of myocardial hypertrophy, coronary artery disease, heart failure, and arrhythmia. Given the proven benefit of β‐blockers in patients with normal kidney function with similar cardiac comorbidities, β‐blockers would seem to be attractive agents to reduce cardiovascular morbidity and mortality in the patient population with advanced chronic kidney disease. However, the value of β‐blockade in patients on chronic dialysis remains unclear. This uncertainty surrounding the efficacy is compounded by the risk of side effects to these patients, such as hypotension, bradycardia, and hyperkalemia. In addition, numerous studies have suggested suboptimal usage of β‐blockers in the dialysis population; this is seen even in high risk patients, such as those with established coronary artery disease. In this review, we will focus on sympathetic nervous system activation in kidney disease and highlight the benefit and risks of β‐blockers usage in the chronic dialysis patient population.
Calcium Balance during Hemodialysis
Authors: McIntyre Christopher W 
Published: October 2007

AbstractCalcium balance during hemodialysis (HD) is important in determining short‐term cardiovascular function, this influences the hemodynamic tolerability of dialysis. In the longer term, calcium flux during HD is an important determinant of overall calcium balance in a patient and may also influence the development and progression of vascular calcification, with its attendant consequences. This article aims to review the assessment and mechanisms of calcium flux during HD, choice of dialysate calcium concentration, influence of HD modality, and potential consequences of therapy choices (cardiovascular and skeletal) resulting from an inappropriate intradialytic calcium balance.
Ultrasound/Fluoroscopy‐Assisted Placement of Peritoneal Dialysis Catheters
Authors: Maya Ivan D. 
Published: October 2007

AbstractPeritoneal dialysis (PD) catheters may be inserted blindly, surgically, and either by laparoscopic, peritoneoscopic, or fluoroscopic approach. A modified fluoroscopic technique by adding ultrasound‐assistance was performed in the present study to ensure entry into the abdominal cavity under direct ultrasound visualization. From March 2005 to May 2007, ultrasound‐fluoroscopic guided placement of PD catheters was attempted in 32 end‐stage renal disease (ESRD) patients. Preoperative evaluation was performed on all patients prior to the procedure. After initial dissection of the subcutaneous tissue anterior to the anterior rectus sheath, the needle was inserted into the abdominal cavity under the guidance of ultrasound. The position of the epigastric artery was also examined using ultrasonography to avoid the risk of arterial injury. PD catheters were successfully placed in 31 of the 32 ESRD patients using this technique. In all of these patients, the needle could be seen entering the abdominal cavity using an ultrasound. In one patient the procedure was abandoned because of bowel puncture by the micro‐puncture needle that was inadvertently advanced into a loop of bowel. This patient did not develop acute abdomen nor needed any intervention. One patient died 4 days after placement of the catheter of unrelated causes. One patient was started on acute peritoneal dialysis the same day of catheter placement without any complications. The rest of the patients started peritoneal dialysis within 2–6 weeks of catheter placement. None of the patients had bleeding related to arterial injury as ultrasound was able to visualize the epigastric artery. Our experience shows that ultrasound‐fluoroscopic technique is minimally invasive and allows for accurate assessment of the entry into the abdominal cavity. This technique can avoid the risk of vascular injury altogether.
Increased Risk of Infection Associated with Polyurethane Dialysis Grafts
Authors: Maya Ivan D. , Weatherspoon Janice , Young Carlton J. , Barker Jill , Allon Michael 
Published: October 2007

AbstractConventional polytetrafluoroethylene (PTFE) dialysis grafts cannot be cannulated for 2–3 weeks following their creation. Polyurethane grafts, made of a self‐sealing material, can be cannulated within 24 hours of implantation, representing a potential advantage in patients with limited catheter options. However, early cannulation may increase the risk of graft infection. We retrospectively queried a prospective, computerized access database to identify 31 patients receiving a polyurethane graft, and 56 date‐matched controls with a PTFE graft. Survival techniques were used to plot graft survival. Thrombosis‐free graft survival (from creation to first thrombosis or failure) was similar for polyurethane and PTFE grafts (1‐year survival, 28%, vs. 32%, p = 0.98). Cumulative graft survival (from creation to permanent failure) was also similar (1‐year survival 42% vs. 52%, p = 0.40). Finally, the cumulative risk of graft infection was 37.5% for polyurethane thigh grafts, 23% for polyurethane upper extremity grafts, 21% for PTFE thigh grafts, and 5% for PTFE upper extremity grafts (p = 0.06 for polyurethane vs. PTFE grafts). The likelihood of thrombosis and failure is similar for polyurethane and PTFE grafts. However, polyurethane grafts may have a higher risk of infection, particularly when they are placed in the thigh. In patients with an access emergency, implantation of a polyurethane graft incurs a tradeoff between earlier cannulation and a higher risk of infection.
Central Vein Cannulation for Hemodialysis: Techniques and Tips for Quick and Safe Temporary Catheter Placement
Authors: Pervez Aslam , Abreo Kenneth 
Published: October 2007

AbstractNephrologists have to place temporary dialysis catheters for hemodialysis in emergency situations. Since there is a dearth of literature on this subject, the authors have written guidelines for the safe and successful placement of these catheters. These instructions should be of help to nephrology trainees who want to master the art of central venous line placement. Based on their experience, the authors have provided a number of tips and techniques for temporary catheter placement in the femoral, internal jugular, and subclavian veins, with and without ultrasound guidance. Patient positioning, preparation of the catheter insertion tray, handling of ultrasound probe, cannulation of the central veins, and guide wire and dilator insertion are described in detail. These guidelines should assist the novice in placing temporary catheters with ease and with minimal complications.
F90927: A New Member in the Class of Cardioactive Steroids
Authors: Keller Markus , Pignier Christophe , Egger Marcel , Niggli Ernst 
Published: October 2007

ABSTRACTF90927 is a newly developed cardioactive drug with a steroid‐like structure. It acts directly and agonistically on the cardiac L‐type Ca2+ channel by shifting its voltage‐dependent activation toward more negative potentials. This leads to an increased influx of Ca2+ and, therefore, to a stronger contraction; however, no arrhythmias occur. Calcium current stimulation can already be observed at nanomolar concentrations, but higher concentrations of F90927 elevate intracellular Ca2+ concentration, causing a reduction of the myocardial compliance and an increased diastolic blood pressure. Vessels also react to F90927 and contract in its presence. Binding of F90927 with the L‐type Ca2+ channel presumably occurs in the vicinity of the transmembrane domains III and IV of the α1 subunit. F90927 exhibits no use dependence and interacts with Ca2+ channel inhibitors of all three known classes of channel modulators (dihydropyridines, phenylalkylamines, and benzothiazepines), suggesting that it is a member of a new class of Ca2+ channel modulators. Due to its adverse effects on blood pressure and vessel contraction, F90927 is not an ideal drug candidate. It has, however, some unique properties, which makes it a promising tool to study the function of the L‐type Ca2+ channel.
The Functional Consequence of the Glu298Asp Polymorphism of the Endothelial Nitric Oxide Synthase Gene in Young Healthy Volunteers
Authors: Godfrey Valerie , Chan Sue‐Lyn , Cassidy Andrew , Butler Robert , Choy AnnaMaria , Fardon Tom , Struthers Allan , Lang Chim 
Published: October 2007

ABSTRACTObjective—To assess the role of the endothelial nitric oxide synthase (eNOS) gene variant as a risk factor for atherosclerosis we sought to investigate whether the Glu298Asp polymorphism of the eNOS gene is associated with functional changes in the endothelium in healthy volunteers. Methods—Endothelial function was assessed in 68 normal volunteers (ages 18–44 years) by bilateral forearm venous occlusion plethysmography with intraarterial infusions of increasing doses of acetylcholine for endothelial‐dependent vasodilation and, with sodium nitroprusside and verapamil for endothelial‐independent vasodilation. Blood was genotyped by polymerase chain reaction and BanII digestion. Results—Asp homozygotes (TT) had a decreased vasodilatory response to acetylcholine [forearm blood flow (FBF) ratio between infused and control arm, 2.82 ± 1.10] when compared to GG variant (FBF ratio to acetylcholine, 3.97 ± 1.90, p= 0.04) and to a certain extent, the GT variant (FBF ratio to acetylcholine, 3.79 ± 2.28, p= 0.07). There was no effect of eNOS genotype on the response to the endothelial‐independent vasodilators—sodium nitroprusside and verapamil. Conclusions—Our data show that carriage of the Asp298 variant of the eNOS gene is associated with a blunted endothelial‐dependent vasodilation in healthy volunteers. These findings support a genetically determined modulation of endothelial dysfunction, a phenotype of early atherosclerosis in humans.
Role of Poly(ADP‐ribose) polymerase 1 (PARP‐1) in Cardiovascular Diseases: The Therapeutic Potential of PARP Inhibitors
Authors: Pacher Pál , Szabó Csaba 
Published: October 2007

ABSTRACTAccumulating evidence suggests that the reactive oxygen and nitrogen species are generated in cardiomyocytes and endothelial cells during myocardial ischemia/reperfusion injury, various forms of heart failure or cardiomyopathies, circulatory shock, cardiovascular aging, diabetic complications, myocardial hypertrophy, atherosclerosis, and vascular remodeling following injury. These reactive species induce oxidative DNA damage and consequent activation of the nuclear enzyme poly(ADP‐ribose) polymerase 1 (PARP‐1), the most abundant isoform of the PARP enzyme family. PARP overactivation, on the one hand, depletes its substrate, NAD+, slowing the rate of glycolysis, electron transport, and ATP formation, eventually leading to the functional impairment or death of the endothelial cells and cardiomyocytes. On the other hand, PARP activation modulates important inflammatory pathways, and PARP‐1 activity can also be modulated by several endogenous factors such as various kinases, purines, vitamin D, thyroid hormones, polyamines, and estrogens, just to mention a few. Recent studies have demonstrated that pharmacological inhibition of PARP provides significant benefits in animal models of cardiovascular disorders, and novel PARP inhibitors have entered clinical development for various cardiovascular indications. Because PARP inhibitors can enhance the effect of anticancer drugs and decrease angiogenesis, their therapeutic potential is also being explored for cancer treatment. This review discusses the therapeutic effects of PARP inhibitors in myocardial ischemia/reperfusion injury, various forms of heart failure, cardiomyopathies, circulatory shock, cardiovascular aging, diabetic cardiovascular complications, myocardial hypertrophy, atherosclerosis, vascular remodeling following injury, angiogenesis, and also summarizes our knowledge obtained from the use of PARP‐1 knockout mice in the various preclinical models of cardiovascular diseases.