bluuebunny/crossref_metadata_2025_split huggingface dataset:
Decreased hemodialysis circuit pressures indicating postpump tubing kinks: A retrospective investigation of hemolysis in five patients
Authors: MALINAUSKAS Richard A. 
Published: July 2008

AbstractThe source of hemolysis during hemodialysis must be quickly identified to avoid life‐threatening complications. At a single clinic, over a 10‐day period in which 550 treatments were performed, 5 case‐patients were retrospectively identified for experiencing acute hemolysis (4 deaths) from an unknown origin. The investigation focused on the postpump arterial tubing as the pressure was not monitored in this region, and the segment was shorter than required and could kink if overly stressed at bend points (i.e., tubing support clips, dialyzer inlet). To determine whether the circuit pressures indicated kinked tubing, a relative comparison between each case‐patient's recorded arterial (prepump) and venous circuit pressures throughout their adverse event treatment and their immediately preceding treatment was conducted. Treatment pressure‐time traces showed that sustained, significant decreases (>25 mmHg) in both of the circuit pressures occurred only on the hemolytic event dates. While direct observations of kinked tubing were not reported, the circuit pressure decreases could only be explained by severe postpump tube kinking causing a decrease in the blood flow rate. While postpump obstructions and hemolysis can occur without causing noticeable changes to the prepump arterial and venous blood line pressures (due to the highly occlusive setting of the roller blood pump), recognizing sudden and/or sustained decreases in the circuit pressures during treatment may help to prevent adverse patient events. This analysis reinforces the importance of regularly checking the blood tubing set for kinks and for monitoring the circuit pressures for atypical trends within and between treatments.
Home hemodialysis in Australia and New Zealand: Practical problems and solutions
Authors: AGAR John W. M. 
Published: July 2008

AbstractHome hemodialysis, as practiced in Australia and New Zealand, offers patients the return of self‐control and self‐esteem. It also allows reconnection with family, friends and (re)employment. Though there are emotional and time‐related “costs” with home hemodialysis, these center on training time, commitment and patient or family stresses and, if carefully managed and properly resourced, can be overcome for most home‐suitable patients. As we believe many center‐based hemodialysis patients are home‐suitable and that home care is severely under‐utilized, assessment techniques to maximize uptake are examined. While patient dropout from home care relates more to staff attitudes than to true home‐failure, dropout is minimized by ensuring the patient and not a carer takes full dialysis responsibility with the carer acting as a supporter and not the facilitator. Installation of home equipment is simple and cheap, the financial costs of home hemodialysis being substantially less than those of facility care where salary and infrastructure costs far exceed training, equipment, installation and maintenance costs at home. Home monitoring is not routinely required especially with longer, more frequent regimens—but effective 24‐hour on‐call nurse and technician cover is essential. Intravenous drug self‐administration at home is safe and effective, reducing the need for hospital visits to a 2–3 monthly minimum. The debilitating effects of facility care cannot be over‐emphasized while the liberating psychology of a well‐supported hemodialysis program is truly satisfying for patient and staff alike.
Short and long nightly hemodialysis in the United States
Authors: LOCKRIDGE Robert S. , PIPKIN Mary 
Published: July 2008

AbstractWhen hemodialysis first started in the United States in the 1960s, a large percentage of patients performed their treatments at home. However, because of reimbursement issues, home hemodialysis (HHD) gradually succumbed to an in‐center approach and eventually a mindset. Since the introduction of nightly HHD by Uldall and Pierratos in 1993, there has been a resurgence of interest in HHD. This paper describes the different types of home hemodialysis being performed as of December 31, 2007 in this country. Because neither the United States Renal Data System (USRDS) nor the End Stage Renal Disease (ESRD) Networks break down home dialysis into the different modalities, a provider questionnaire was sent out to 2 major providers, a number of mid‐level providers and other providers known to do HHD. In addition, a questionnaire was sent out to 3 machine providers to obtain the number of patients using their machine for HHD as of December 31, 2007. The results showed that 91.7% of patients are dialyzing in‐center, 7.3% are doing peritoneal dialysis, and 0.7% are doing HHD. Currently about 1% of ESRD patients in the United States are doing home hemodialysis. NxStage, however, has started 1000 patients in the past year on short‐daily home hemodialysis. Patients are beginning to understand that there are better options than 3 times a week in‐center dialysis. And as a result of the “HEMO Study,” nephrologists now believe that longer and more frequent dialysis is a better therapy for ESRD patients. Therefore, promotion of HHD should become a priority for the renal community in the future.
Acute heart inflammation: ultrastructural and functional aspects of macrophages elicited by Trypanosoma cruzi infection
Authors: Melo Rossana C. N. 
Published: July 2008

Introduction
Acute T. cruzi infection induces accentuated mobilization/migration of monocytic lineage cells into heart
Heart inflammatory macrophages show a distinct morphology and are actively involved in parasite phagocytosis
Lipid bodies as structural markers of inflammatory macrophages
Macrophages and the resolution of acute inflammation and heart repair
Concluding remarks

AbstractThe heart is the main target organ of the parasite Trypanosoma cruzi, the causal agent of Chagas' disease, a significant public health issue and still a major cause of morbidity and mortality in Latin America. During the acute disease, tissue damage in the heart is related to the intense myocardium parasitism. To control parasite multiplication, cells of the monocytic lineage are highly mobilized. In response to inflammatory and immune stimulation, an intense migration and extravasation of monocytes occurs from the bloodstream into heart. Monocyte differentiation leads to the formation of tissue phagocytosing macrophages, which are strongly activated and direct host defence. Newly elicited monocyte‐derived macrophages both undergo profound physiological changes and display morphological heterogeneity that greatly differs from originally non‐inflammatory macrophages, and underlie their functional activities as potent inflammatory cells. Thus, activated macrophages play a critical role in the outcome of parasite infection. This review covers functional and ultrastructural aspects of heart inflammatory macrophages triggered by the acute Chagas' disease, including recent discoveries on morphologically distinct, inflammation‐related organelles, termed lipid bodies, which are actively formed in vivo within macrophages in response to T. cruzi infection. These findings are defining a broader role for lipid bodies as key markers of macrophage activation during innate immune responses to infectious diseases and attractive targets for novel anti‐inflammatory therapies. Modulation of macrophage activation may be central in providing therapeutic benefits for Chagas' disease control.
PPARγ2 expression in growth plate chondrocytes is regulated by p38 and GSK‐3
Authors: Stanton Lee‐Anne , Li Jennifer Ruizhe , Beier Frank 
Published: July 2008

AbstractAlthough peroxisome proliferator activated receptor (PPAR)γ remains a critical regulator of preadipocyte differentiation, new roles have been discovered in inflammation, bone morphogenesis, endothelial function, cancer, longevity and atherosclerosis. Despite the demonstration of PPARγ expression in chondrocytes, its role and the pathways affecting its expression and activity in chondrocytes remain largely unknown. We investigated the effects of PPARγ activation on chondrocyte differentiation and its participation in chondrocyte lipid metabolism. PPARγ2 expression is highly regulated during chondrocyte differentiation in vivo and in vitro PPARγ activation with troglitazone resulted in increased Indian hedgehog expression and reduced collagen X expression, confirming previously described roles in the inhibition of differentiation. However, the major effect of PPARγ2 in chondrocytes appears to be on lipid metabolism. During differentiation chondrocytes increase expression of the lipid‐associated metabolizing protein, Lpl, which is accompanied by increased gene expression of PPARγ. PPARγ expression is suppressed by p38 activity, but requires GSK‐3 activity. Furthermore, Lpl expression is regulated by p38 and GSK‐3 signalling. This is the first study demonstrating a relationship between PPARγ2 expression and chondrocyte lipid metabolism and its regulation by p38 and GSK‐3 signalling.
Genetic transfer of fusion proteins effectively inhibits VCAM‐1‐mediated cell adhesion and transmigration via inhibition of cytoskeletal anchorage
Authors: Hagemeyer Christoph E. , Ahrens Ingo , Bassler Nicole , Dschachutaschwili Natia , Chen Yung C. , Eisenhardt Steffen U. , Bode Christoph , Peter Karlheinz 
Published: July 2008

AbstractThe adhesion of leukocytes to endothelium plays a central role in the development of atherosclerosis and thus represents an attractive therapeutic target for anti‐atherosclerotic therapies. Vascular cell adhesion molecule‐1 (VCAM‐1) mediates both the initial tethering and the firm adhesion of leukocytes to endothelial cells. Our work evaluates the feasibility of using the cytoskeletal anchorage of VCAM‐1 as a target for gene therapy. As a proof of concept, integrin αIIbβ3‐mediated cell adhesion with clearly defined cytoskeletal anchorage was tested. We constructed fusion proteins containing the intracellular domain of β3 placed at various distances to the cell membrane. Using cell adhesion assays and immunofluorescence, we established fusion constructs with competitive and dominant negative inhibition of cell adhesion. With the goal being the transfer of the dominant negative mechanism towards VCAM‐1 inhibition, we constructed a fusion molecule containing the cytoplasmic domain of VCAM‐1. Indeed, VCAM‐1 mediated leukocyte adhesion can be inhibited via transfection of DNA encoding the designed VCAM‐1 fusion protein. This is demonstrated in adhesion assays under static and flow conditions using CHO cells expressing recombinant VCAM‐1 as well as activated endothelial cells. Thus, we are able to describe a novel approach for dominant negative inhibition of leukocyte adhesion to endothelial cells. This approach warrants further development as a novel gene therapeutic strategy that aims for a locally restricted effect at atherosclerotic areas of the vasculature.
IL‐12 immunotherapy of murine leukaemia: comparison of systemic versus gene modified cell therapy
Authors: Labbe Alain , Nelles Megan , Walia Jagdeep , Jia Lintao , Furlonger Caren , Nonaka Takahiro , Medin Jeffrey A. , Paige Christopher J. 
Published: July 2008

AbstractThe ability of IL‐12 to initiate anti‐leukaemia immune responses has been well established; however clinical outcomes fail to recapitulate the therapeutic benefits observed in the laboratory. To address this, we compared two systems of IL‐12 therapy that elicit protective immune responses against the murine acute lymphoblastic leukaemia (ALL) cell line, 70Z/3. These systems differ in the method of IL‐12 administration and ultimately result in leukaemia clearance by distinct mechanisms, emphasizing the importance of treatment vehicle. Injecting low‐dose IL‐12 was sufficient to elicit long‐term protective immunity against an established leukaemia burden, mediated by both CD4+ and CD8+ T cells. These findings agree with the standard model of IL‐12 activity. We compared this protocol to a cell‐based approach in which a novel lentiviral vector (LV) expressing murine IL‐12 was created, 70Z/3 cells transduced, and clones selected that stably secrete different amounts of IL‐12. We found that only a small proportion (1%) of IL‐12 secreting cells were required for rejection but that the amount of IL‐12 produced per cell was critical for successful therapy. Importantly, the levels of IL‐12 required were found to be higher than the levels reported to date in the human clinical trial literature. We found that the cell‐based approach led to protective immunity that was both long‐term and specific but dependent primarily on a CD4+ cellular subset alone. Our results highlight that the mode of IL‐12 delivery has a distinct impact on the immune response initiated, leading to leukaemia clearance by disparate mechanisms. We also establish a new and critical parameter, IL‐12 production/cell, which may have significant implications for future therapeutic design.
Activation of protease calpain by oxidized and glycated LDL increases the degradation of endothelial nitric oxide synthase
Authors: Dong Yunzhou , Wu Yong , Wu Mingyuan , Wang Shuangxi , Zhang Junhua , Xie Zhonglin , Xu Jian , Song Ping , Wilson Kenneth , Zhao Zhengxing , Lyons Timothy , Zou Ming‐Hui 
Published: July 2008

AbstractOxidation and glycation of low‐density lipoprotein (LDL) promote vascular injury in diabetes; however, the mechanisms underlying this effect remain poorly defined. The present study was conducted to determine the effects of ‘heavily oxidized’ glycated LDL (HOG‐LDL) on endothelial nitric oxide synthase (eNOS) function. Exposure of bovine aortic endothelial cells with HOG‐LDL reduced eNOS protein levels in a concentration‐ and time‐dependent manner, without altering eNOS mRNA levels. Reduced eNOS protein levels were accompanied by an increase in intracellular Ca2+, augmented production of reactive oxygen species (ROS) and induction of Ca2+‐dependent calpain activity. Neither eNOS reduction nor any of these other effects were observed in cells exposed to native LDL. Reduction of intracellular Ca2+ levels abolished eNOS reduction by HOG‐LDL, as did pharmacological or genetic through calcium channel blockers or calcium chelator BAPTA or inhibition of NAD(P)H oxidase (with apocynin) or inhibition of calpain (calpain 1‐specific siRNA). Consistent with these results, HOG‐LDL impaired acetylcholine‐induced endothelium‐dependent vasorelaxation of isolated mouse aortas, and pharmacological inhibition of calpain prevented this effect. HOG‐LDL may impair endothelial function by inducing calpain‐mediated eNOS degradation in a ROS‐ and Ca2+‐dependent manner.
Chitosan cooperates with mesenchyme‐derived factors inregulating salivary gland epithelial morphogenesis
Authors: Yang Tsung‐Lin , Young Tai‐Horng 
Published: July 2008

AbstractChitosan is a widely used biocompatible biomaterial in the tissue regeneration, but its utility and application in the tissue morphogenesis of salivary gland remains unclear. The study aimed to explore the effects of chitosan on the epithelial morphogenesis of submandibular gland (SMG). With chitosan, the branching morphogenesis of the whole SMG explant was facilitated, and the morphogenetic‐promoting effects of mesenchymal tissue on SMG were further enhanced. Furthermore, chitosan was competent to induce recombined SMG epithelium to form branches in the serum‐free condition independently. In the presence of chitosan, the morphogenetic efficacy of mesenchyme‐derived growth factors responsible for epithelial morphogenesis including fibroblast growth factors 7, fibroblast growth factor 10 and hepatocyte growth factor increased. The specific epithelial phenotype induced by individual growth factor, which was required for the accomplishment of salivary epithelial morphogenesis, was promoted by chitosan. Moreover, the proliferative and the chemotactic properties of these growth factors towards the SMG epithelia were also reinforced by chitosan. Therefore, in orchestrating and intensifying the essential mesenchyme‐derived growth factors, chitosan is versatile in mediating SMG epithelium to form a predetermined phenotype more efficiently and comprehensively. This study suggested that chitosan is a morphogenetic‐regulating biomaterial for salivary tissue, which might be useful for the future salivary gland investigation and regeneration.
5‐year clinical experience with BTI® dental implants: risk factors for implant failure
Authors: Anitua Eduardo , Orive Gorka , Aguirre José Javier , Ardanza Bruno , Andía Isabel 
Published: July 2008

AbstractObjectives: The aims of this study were to identify with appropriate statistical tests the risk factors associated with implant failure and to evaluate the long‐term survival of dental implants using implant loss as an outcome variable and performing an implant‐, surgery‐ and patient‐based analysis of failures.Material and Methods: A retrospective cohort study design was used. One thousand sixty patients received 5787 BTI® implants during the years of 2001–2005 in Vitoria, Spain. The potential influence of demographic items, clinical items, surgery‐dependent items and prosthetic variables on implant survival was studied. Implant survival was analysed using a life‐table analysis. Cox proportional hazards regression was used to identify risk factors related to implant failure.Results: Smoking habits, implant position, implant staging (two‐stage implants) and the implementation of special techniques were statistically correlated with lower implant survival rates. Two risk factors associated with implant failure were detected in this study: implant staging (two‐stage implants) and the use of special techniques. Additionally, the overall survival rates of BTI® implants were 99.2%, 96.4% and 96% for the implant‐, surgery‐ and patient‐based analysis, respectively. Totally, 28 out from 5787 implants (0.48%) were lost during the observation period. Most of the patients with implant failure (69.6%) presented chronic or aggressive periodontitis.Conclusions: Implant staging and the use of special techniques are risk factors for implant failure.
Clonal stability of Porphyromonas gingivalis in untreated periodontitis
Authors: Van Winkelhoff Arie J. , Rijnsburger Martine C. , Van Der Velden Ubele 
Published: July 2008

AbstractObjectives: The objective of the present investigation was to study the clonal stability of Porphyromonas gingivalis in a population of Indonesian subjects, deprived of dental care and with varying degrees of periodontitis over a period of 8 years.Material and Methods: In 1994, 105 subjects and in 2002, 103 subjects were P. gingivalis culture positive. Multiple isolates from each of these subjects were used for amplified fragment length polymorphism (AFLP) typing.Results: Sixty‐six individuals were P. gingivalis culture positive at both time points. In 31 subjects (47%) an exact identical P. gingivalis genotype distribution was found in 1994 and in 2002. In 26 of these subjects one genotype, in eight subjects two identical genotypes were found at both time points. In 70% of the subjects at least one P. gingivalis genotype was found in 1994 and 2002, whereas other genotypes were either newly detected or were no longer detectable. Identical genotypes were found in 26% of the sibships. Clonal stability in siblings was 39%. Horizontal transmission of P. gingivalis was only found in 2002 and was low (11%). In total, 56 P. gingivalis genotypes were identified in 1994 and 61 in 2002. Twenty‐four appeared unique, whereas other genotypes were found in multiple subjects within as well as without families. One genotype occurred in 11 different subjects.Conclusions: The clonal stability of P. gingivalis under natural conditions is high. Complete different genotype distribution was found in only 27% of the subjects. Transmission of P. gingivalis occurred frequently among siblings but not among spouses.
Atrophoderma of Pasini and Pierini: a clinical and histopathological study
Authors: Saleh Zenus , Abbas Ossama , Dahdah Maurice J. , Kibbi Abdul G. , Zaynoun Shukrallah , Ghosn Samer 
Published: July 2008

Background:  Idiopathic atrophoderma of Pasini and Pierini (IAPP) usually manifests as one or multiple depressed and hyperpigmented patches, with a predilection to the trunk. No diagnostic changes are usually seen on histology. Elastic stains often reveal no abnormalities.Objective:  To review our cases of IAPP, describe their clinical and histological findings and compare them with the literature.Methods:  Retrospective review of IAPP cases who presented to our institution between 1994 and 2006.Results:  From a total of 16 patients, only 19% displayed hyperpigmented lesions, while 81% had either hypopigmented (9/16) or skin‐colored (4/16) lesions. The sites predominantly affected were the lower extremities (62.5%), followed by the upper extremities and trunk. Only in one patient was IAPP co‐existent with morphea. Histology revealed no diagnostic abnormalities; however, elastic stains showed a spectrum of changes ranging from normal to severe diminution and fragmentation of elastic fiber network.Conclusions:  Our study shows several new aspects of IAPP. Clinically, the lesions were most commonly hypopigmented and involved predominantly the extremities. Histologically, IAPP exhibited a spectrum of alterations in elastic fibers. The most prevalent form of IAPP in our country seems to be unassociated with morphea.
Myocardial infarction in thrombotic thrombocytopenic purpura: a single‐center experience and literature review
Authors: Wahla Ali S. , Ruiz Jimmy , Noureddine Nizar , Upadhya Bharathi , Sane David C. , Owen John 
Published: July 2008

AbstractBackground:  Several case reports and series have described myocardial infarctions (MIs) in patients hospitalized for thrombotic thrombocytopenic purpura (TTP). The exact magnitude and outcome of this complication are unknown.Methods:  Electronic medical records for patients admitted to Wake Forest University Baptist Medical Center were examined from 1996 to 2005. Those patients having a diagnosis of TTP during the hospitalization period were included in the analysis. Only patients’ initial episodes of TTP were analyzed. Baseline cardiac and TTP risk factors were documented. Outcomes analyzed included MIs, arrhythmias, development of congestive heart failure and death.Results:  Eighty‐five patients diagnosed with TTP were identified with 13 (15.3%) having MIs, as defined by an elevation of cardiac enzymes. Median troponin I value was 5.9 ng/mL (range 3.7–8.8 ng/mL). Twelve patients had non‐ST segment elevation MIs and one had ST segment elevation. Two of 13 patients who had echocardiographic analysis had documented wall motion abnormalities. There was no difference between non‐MI and MI patients in cardiac risk factors, prior cardiac events, history of thromboembolic disease or heart failure. There was no in‐hospital mortality difference.Conclusion:  MI is an important complication of TTP, identified in 15.3% of patients in our study. Routine cardiovascular evaluation with cardiac enzymes, electrocardiography, and telemetry is warranted in acute TTP patients. Appropriate intervention is yet to be determined.