bluuebunny/crossref_metadata_2025_split huggingface dataset:
Implementation of buffy coat platelet component production: comparison to platelet‐rich plasma platelet production
Authors: Levin Elena , Culibrk Brankica , Gyöngyössy‐Issa Maria I. C. , Weiss Sandra , Scammell Kenneth , LeFresne Wanda , Jenkins Craig , Devine Dana V. 
Published: July 2008

BACKGROUND: Buffy coat (BC) production of platelets (PLTs) has been successfully used in Europe for more than two decades. Currently, Canadian Blood Services is implementing the BC method. This article summarizes results of the validation testing performed to qualify the process of PLT production from whole blood and compares the quality of PLTs produced in routine production by either the PLT‐rich plasma method (PRP‐PCs) or the BC method (BC‐PCs).STUDY DESIGN AND METHODS: Validation data included variables used for routine quality control (QC; pH, PLT count, volume, sterility, residual white blood cell count) as well as nonroutine testing of PLTs for PLT activation, metabolic changes during storage, and PLT responsiveness to hypotonic shock and the extent of shape change induced by adenosine 5′‐diphosphate. BC‐PCs were tested on Days 1 and 6. QC of production runs included the same routine tests performed on Day 6.RESULTS: PLTs produced by the BC method during validation and pilot implementation met all Canadian Standards Association standards with respect to yield, volume, pH, and leukoreduction. Additional validation testing indicated a moderate level of PLT storage lesion development. In comparison to PRP‐PCs, in vitro variables of BC‐PCs, either pH in this study, or other markers compared to the literature were better, suggesting that BC‐PCs have less evidence of production‐related damage and improved PLT quality during storage.CONCLUSIONS: PLT concentrates produced from whole blood by the BC method after an overnight hold have laboratory variables suggestive of a higher quality than those concentrates produced by the PRP method.
Exercise and dialysis
Authors: JOHANSEN Kirsten L. 
Published: July 2008

AbstractFortunately, the literature on exercise among patients on hemodialysis has grown too broad to be included in a single review. The focus of this review is on interventional studies, with an emphasis on those studies that included a control group. The good news is that there is ample evidence that exercise can improve fitness (VO2 peak), physical functioning, and some cardiovascular risk factors in the dialysis population. However, there have been few comparative studies, and there is no consensus regarding the most beneficial regimen or the one most acceptable to large numbers of patients. A new set of recommendations from the American College of Sports Medicine and the American Heart Association for older individuals and individuals with chronic diseases is relevant for our patient population and can be used to guide exercise prescription until disease‐specific data are available to fill the gap.
Dialysis Disequilibrium Syndrome presenting as a focal neurological deficit
Authors: ATTUR Ravindra Prabhu , KANDAVAR Ramprasad , KADAVIGERE Rajagopal , BAIG Waqas Wahid 
Published: July 2008

AbstractWe report a patient suffering from chronic kidney disease who presented to us with severe pulmonary edema. His clinical, laboratory, and sonological parameters were suggestive of end‐stage renal disease. Hemodialysis was initiated, and after 48 hours (3 sessions of hemodialysis) he became drowsy and a neurological examination revealed left upper limb monoplegia with left facial palsy. Urgent computerized tomography scan of the brain revealed diffuse hypodensity in the cerebral white matter bilaterally, and brain magnetic resonance imaging showed diffuse hyperintensity in the cerebral white matter bilaterally, right internal capsule and external capsule on fluid attenuated inversion recovery and T2 sequences (hypointense on T1 sequence). He made a gradual but complete neurological recovery and was discharged 2 weeks later with normal neurological status. A repeat brain magnetic resonance imaging on follow‐up 6 weeks later revealed complete resolution of the white matter abnormalities.
Hepatitis B and C in dialysis units in Iran: Changing the epidemiology
Authors: ALAVIAN Seyed Moayed , BAGHERI‐LANKARANI Kamran , MAHDAVI‐MAZDEH Mitra , NOUROZI Shahram 
Published: July 2008

AbstractHepatitis B (HBV) and C (HCV) viruses are the most important infections transmitted by the parenteral route in patients receiving maintenance dialysis. The prevalence varies markedly from country to country. The aim of this study is to review the efficacy of the strategies to reduce the incidence of these infections and the trend of results in Iran. As a routine, all hemodialysis patients in Iran have biannual blood samples for assessment of serum HBSAg, HBS Abs, and HCV Abs. The data are collected in the Ministry of Health. For statistical analysis, prevalence, and incidence were calculated. There is an increasing prevalence/incidence of end‐stage renal disease (ESRD) in Iran, from 238/49.9 pmp in 2000 to 357/63.8 pmp in 2006. The prevalence of positive HBSAg and HCV Abs decreased from 3.8% and 14.4% in 1999 to 2.6% and 4.5% in 2006, respectively. Regarding the genotype distribution in Iran, no one was found with genotype 2. On the subject of decreasing HBV infection, our next strategy should be mandatory vaccination in dialysis centers and in the pre‐ESRD period. Concerning HCV infection prevention, 2 approaches may be recommended: the first is decrease of duration of the hemodialysis period by possible early transplantation of suitable patients. The next is a strictly enforced isolation policy for HCV‐positive patients, which may play a role in limiting HCV transmission in HD units, and universal precaution in dialysis units should be under constant close surveillance.
The renaissance of home hemodialysis: Where we are, why we got here, what is happening in the United States and elsewhere
Authors: BLAGG Christopher R. 
Published: July 2008

AbstractHome hemodialysis has been around since 1964, but its use has declined over the years in most countries, this despite its advantages, particularly improved patient survival and quality of life and significant cost savings. Experience has shown that home hemodialysis can be performed successfully by many more patients than at present. Recently, with the demonstration of even better results with more frequent hemodialysis that is obviously best performed at home and with the development of new, more patient‐friendly machines, the use of home hemodialysis is beginning to increase again.
The advantages and disadvantages of home hemodialysis
Authors: MASTERSON Rosemary 
Published: July 2008

AbstractIn Australia, 12% of the hemodialysis population dialyze at home. Until recently, the majority of these patients dialyzed for similar hours to those in satellite dialysis. However, in the past 5 years there has been a new departure such that in many centers the concept of home hemodialysis is now synonymous with extended hours dialysis. Registry data supports the concept that increased frequency and duration of dialysis may result in improved patient survival and a reduction in cardiovascular risk profile. It is hoped, therefore, that the long recognized survival benefit observed in home hemodialysis patients may be further augmented by the swing to extended hours dialysis in this patient population. In addition to the physiological benefits of extended hours home dialysis, there are clear quality of life, social, and economic advantages associated with dialyzing at home. There are however a number of perceived disadvantages to home hemodialysis including the application and time commitment required for training, the potential for relationship strain or “burnout,” and reluctance to “hospitalize” the home. Overall, however, in this new era of extended hours dialysis, the advantages both physiological and lifestyle of home hemodialysis far outweigh the disadvantages.
Complications of home hemodialysis
Authors: HAWLEY Carmel M. , JEFFRIES Janine , NEARHOS Jane , VAN EPS Carolyn 
Published: July 2008

AbstractHome hemodialysis is regaining popularity as a treatment choice for end‐stage kidney disease. This trend is fueled by numerous reports of better survival and improved quality of life with primarily home‐based more frequent and/or longer hours of hemodialysis. Home hemodialysis in the contemporary era is generally very safe. Advances in machine technology have reduced technical complications and longer and more frequent treatments have reduced the risk of hypotension and cardiovascular instability. A successful home hemodialysis program must focus on patient safety to prevent serious hemorrhage from needle dislodgement and enable an aseptic cannulation technique. In addition, vigilance in relation to machine maintenance procedures and attention to water quality are key skills that patients must acquire for optimal outcomes. The possibility of increased septic events with longer and more frequent hemodialysis regimens performed in the home, the long‐term psychosocial effects of home hemodialysis, and the best methods for maintaining compliance of patients in the long term are of particular contemporary interest.
A molecular study of pathways involved in the inhibition of cell proliferation in neuroblastoma B65 cells by the GSK‐3 inhibitors lithium and SB‐415286
Authors: Pizarro Javier G. , Folch Jaume , Esparza José Luis , Jordan J. , Pallàs Mercè , Camins Antoni 
Published: July 2008

AbstractPharmacological GSK‐3 inhibitors are potential drugs for the treatment of neurodegenerative diseases, cancer and diabetes. We examined the antiproliferative effects of two GSK‐3 inhibitors, lithium and SB‐415286, on B65 neuroblastoma cell line. Treatment of B65 cells with either drug administered separately caused a decrease in cell proliferation that was associated with G2/M cell cycle arrest. Cell‐cycle proteins such as cyclins D, E, A, cdk4 and cdk2 were up‐regulated. Since lithium and SB‐415286‐induced G2/M arrest we studied changes in the expression of proteins involved in this phase, specifically cyclin B, cdc2 and the phosphorylated form of this protein (tyr15‐cdc2). Both drugs increased the expression of tyr15‐cdc2, thus inhibiting mitosis. On the other hand, SB‐415286 increased the expression of SIRT2, involved in the regulation of proliferation. Moreover, cell‐cycle arrest mediated by SB‐415286 was accompanied by apoptosis that was not prevented by 100 μM of zVAD‐fmk (benzyloxycarbonyl‐Val‐Ala‐Asp‐fluoromethylketone), a pan‐caspase inhibitor. Likewise, GSK‐3 inhibitors did not affect the mitochondrial release of apoptosis inducing factor (AIF). We conclude that inhibitors of GSK‐3 induced cell‐cycle arrest, mediated by the phosphorylation of cdc2 and, in the case of SB‐415286, SIRT2 expression, which induced apoptosis in a caspase‐independent manner.
Combined R‐α–lipoic acid and acetyl‐L‐carnitine exerts efficient preventative effects in a cellular model of Parkinson’s disease
Authors: Zhang Hongyu , Jia Haiqun , Liu Jianghai , Ao Ni , Yan Bing , Shen Weili , Wang Xuemin , Li Xin , Luo Cheng , Liu Jiankang 
Published: July 2008

AbstractMitochondrial dysfunction and oxidative damage are highly involved in the pathogenesis of Parkinson’s disease (PD). Some mitochondrial antioxidants/nutrients that can improve mitochondrial function and/or attenuate oxidative damage have been implicated in PD therapy. However, few studies have evaluated the preventative effects of a combination of mitochondrial antioxidants/nutrients against PD, and even fewer have sought to optimize the doses of the combined agents. The present study examined the preventative effects of two mitochondrial antioxidant/nutrients, R‐α–lipoic acid (LA) and acetyl‐L‐carnitine (ALC), in a chronic rotenone‐induced cellular model of PD. We demonstrated that 4‐week pretreatment with LA and/or ALC effectively protected SK‐N‐MC human neuroblastoma cells against rotenone‐induced mitochondrial dysfunction, oxidative damage and accumulation of α‐synuclein and ubiquitin. Most notably, we found that when combined, LA and ALC worked at 100–1000‐fold lower concentrations than they did individually. We also found that pretreatment with combined LA and ALC increased mitochondrial biogenesis and decreased production of reactive oxygen species through the up‐regulation of the peroxisome proliferator‐activated receptor‐γ coactivator 1α as a possible underlying mechanism. This study provides important evidence that combining mitochondrial antioxidant/nutrients at optimal doses might be an effective and safe prevention strategy for PD.
Lysophosphatidylcholine up‐regulates human endothelial nitric oxide synthase gene transactivity by c‐Jun N‐terminal kinase signalling pathway
Authors: Xing Feiyue , Liu Jing , Mo Yongyan , Liu Zhifeng , Qin Qinghe , Wang Jingzhen , Fan Zhenhua , Long Yutian , Liu Na , Zhao Kesen , Jiang Yong 
Published: July 2008

AbstractHuman endothelial nitric oxide synthase (eNOS) plays a pivotal role in maintaining blood pressure homeostasis and vascular integrity. It has recently been reported that mitogen‐activated protein kinases (MAPKs) are intimately implicated in expression of eNOS. However detailed mechanism mediated by them remains to be clarified. In this study, eNOS gene transactivity in human umbilical vein endothelial cells was up‐regulated by stimulation of lysophosphatidylcholine (LPC). The stimulation of LPC highly activated both extracellular signal‐regulated kinase 1/2 (ERK1/2) and c‐Jun N‐terminal kinase (JNK), with differences in the dynamic processes of activation between them. Unexpectedly, p38 MAPK could not be activated by the stimulation of LPC. The activation of JNK signalling pathway by overexpression of JNK or its upstream kinase active mutant up‐regulated the transactivity of eNOS significantly, but the activation of p38 signalling pathway down‐regulated it largely. The inhibition of either ERK1/2 or JNK signalling pathway by kinase‐selective inhibitors could markedly block the induction of the transactivity by LPC. It was observed by electrophoretic mobility shift assay that LPC stimulated both SP1 and AP1 DNA binding activity to go up. Additionally using decoy oligonucleotides proved that SP1 was necessary for maintaining the basal or stimulated transactivity, whereas AP1 contributed mainly to the increase of the stimulated transactivity. These findings indicate that the up‐regulation of the eNOS gene transactivity by LPC involves the enhancement of SP1 transcription factor by the activation of JNK and ERK1/2 signalling pathways and AP1 transcription factor by the activation of JNK signalling pathway.
Acitretin induces apoptosis through CD95 signalling pathway in human cutaneous squamous cell carcinoma cell line SCL‐1
Authors: Lin Xiu‐Ying , He Chun‐Di , Xiao Ting , Jin Xin , Chen Jiang , Wang Ya‐Kun , Liu Mei , Wang Kai‐Bo , Jiang Yi , Wei Hua‐Chen , Chen Hong‐Duo 
Published: July 2008

AbstractSkin cancers are by far the most common human malignancies. Retinoids have shown promising preventive and therapeutic effects against a variety of human malignancies. The aim of this study was to investigate the apoptosis‐inducing effect of acitretin on human skin squamous cell carcinoma (SCC) SCL‐1 cells. We found that acitretin preferentially inhibited the growth of SCL‐1 cells in a dose‐ and time‐dependent manner, but not of non‐malignant keratinocyte HaCaT cells. This inhibition appeared to be due to induction of apoptosis as revealed by enzyme‐linked immunosorbent assay. AnnexinV/propidium iodide assay and morphological observation confirmed the pro‐apoptotic effect of acitretin on SCL‐1 cells. We further demonstrated that apoptosis was induced within 1–2 days and involved activation of caspases‐8, ‐9, ‐3 and poly (ADP‐ribose) polymerase (PARP). Caspase‐8 inhibitor effectively suppressed acitretin‐induced apoptosis whereas caspase‐9 inhibitor did not. Acitretin increased the levels of CD95 (Fas), CD95‐ligand and Fas‐associated death domain. Neutralizing ZB4 anti‐Fas antibody significantly inhibited the apoptosis in SCL‐1 cells induced by acitretin. These results suggest that acitretin is able to induce apoptosis in skin cancer cells possibly via death receptor CD95 apoptosis pathway without affecting the viability of normal keratinocyte.
Hypoxia response and microRNAs: no longer two separate worlds
Authors: Ivan Mircea , Harris Adrian L. , Martelli Fabio , Kulshreshtha Ritu 
Published: July 2008

Introduction: miRs, small molecules with wide impact
A role for hypoxia in the regulation of miR expression
Role of HIF in the regulation of miR‐210
The ongoing search for miR‐210 targets
Perspectives: towards clinical applications of miR‐210 manipulation

AbstractMicroRNAs (miRs) are short non‐coding transcripts involved in a wide variety of cellular processes. Several recent studies have established a link between hypoxia, a well‐documented component of the tumour microenvironment, and specific miRs. One member of this class, miR‐210, was identified as hypoxia inducible in all the cell types tested, and is overexpressed in most cancer types. Its hypoxic induction is dependent on a functional hypoxia‐inducible factor (HIF), thus extending the transcriptional repertoire of the latter beyond ‘classic’ genes. From a clinical standpoint, miR‐210 overexpression has been associated with adverse prognosis in breast tumours and been detected in serum of lymphoma patients and could serve as a tool to define hypoxic malignancies. We discuss the role of miR‐210 and its emerging targets, as well as possible future directions for clinical applications in oncology and ischaemic disorders.
microRNAs: tiny regulators of synapse function in development and disease
Authors: Bicker Silvia , Schratt Gerhard 
Published: July 2008

Introduction
miRNA biogenesis and mode of action
Regulation of miRNA expression
miRNAs as regulators in the developing nervous system
Synapse development and plasticity in vertebrates
miRNAs as regulators in post‐mitotic neurons
miRNA transport to the dendrite
miRNAs in diseases of the nervous system
Diagnostic and therapeutic persDiagnostic and therapeutic perspectives
Conclusion

AbstractThe development and function of neuronal circuits within the brain are orchestrated by sophisticated gene regulatory mechanisms. Recently, microRNAs have emerged as a novel class of small RNAs that fine‐tune protein synthesis. microRNAs are abundantly expressed in the vertebrate nervous system, where they contribute to the specification of neuronal cell identity. Moreover, microRNAs also play an important role in mature neurons. This review summarizes the current knowledge about the function of microRNAs in the nervous system with special emphasis on synapse formation and plasticity. The second part of this work will discuss the potential involvement of microRNAs in neurologic diseases. The study of brain microRNAs promises to expand our understanding of the mechanisms underlying higher cognitive functions and neurologic diseases.
Neuronal cell death in neurodegenerative diseases: recurring themes around protein handling
Authors: Gorman Adrienne M. 
Published: July 2008

AbstractNeuronal cell death plays a role in many chronic neurodegenerative diseases with the loss of particular subsets of neurons. The loss of the neurons occurs during a period of many years, which can make the mode(s) of cell death and the initiating factors difficult to determine.In vitroandin vivomodels have proved invaluable in this regard, yielding insight into cell death pathways. This review describes the main mechanisms of neuronal cell death, particularly apoptosis, necrosis, excitotoxicity and autophagic cell death, and their role in neurodegenerative diseases such as ischaemia, Alzheimer's, Parkinson's and Huntington's diseases. Crosstalk between these death mechanisms is also discussed. The link between cell death and protein mishandling, including misfolded proteins, impairment of protein degradation, protein aggregation is described and finally, some pro‐survival strategies are discussed.
Differential bone marrow stem cell mobilization by G‐CSF injection or arterial ligation in baboons
Authors: Shi Qiang , Hodara Vida , Butler Stephanie D. , Thomas III Charles A. , Hubbard Gene B. , VandeBerg John L. , Wang Xing L. 
Published: July 2008

AbstractBone marrow stem cells (BMSCs) are mobilized in response to ischemic attacks, e.g. myocardial infarction, to repair the damage, or by cytokines, e.g. granulocyte colony‐stimulating factor (G‐CSF), which is used to harvest BMSCs for autologous transplantation. In order to optimize BMSC mobilization strategy for cardiovascular repair, we investigated whether BMSCs mobilized by G‐CSF share the same subtype profile as that by ischemia in a non‐human primate model. We subjected five baboons to subcutaneous G‐CSF injection and five baboons to femoral artery ligation. Blood BMSCs were measured by surface antigens; functional differentiation to endothelial cells (ECs) was assessed by colony‐forming capacity, expression of mature EC antigens and tube‐like formation. The number of circulating CD34+/CD45RA− cells spiked on day 3 post‐stimulation in both groups. While the number of CD34+ cells released by artery ligation was 2‐fold lower by comparison with the number released by G‐CSF administration, significantly more CD133+/KDR+/CXCR4+/CD31+ cells were detected in the baboons that underwent artery ligation. After culture in endothelial growth medium, mononuclear cells from baboons with artery ligation formed more EC colonies and more capillary‐like tubes (P < 0.05), expressed higher vWF and phagocytosed more Dil‐Ac‐LDL (P < 0.05). While G‐CSF and artery ligation can mobilize BMSCs capable of differentiating into ECs, BMSCs mobilized by the artery ligation simulating in vivo ischemic attacks have higher potential for vascular differentiation. Our findings demonstrate that different mobilization forces release different sets of BMSCs that may have different capacity for cardiovascular differentiation.
Interleukin‐6 and leptin as markers of energy metabolicchanges in advanced ovarian cancer patients
Authors: Macciò Antonio , Madeddu Clelia , Massa Daniela , Astara Giorgio , Farci Daniele , Melis Gian Benedetto , Mantovani Giovanni 
Published: July 2008

AbstractThe progression of the neoplastic disease is characterized by specific alterations of energy metabolism and by symptoms like fatigue, anorexia, nausea, anaemia, immunodepression and poor performance status (PS). The main cause of these symptoms and metabolic abnormalities is the chronic action of proinflammatory cytokines released both by tumour and immune cells. The present study aimed to assess the relationship between markers of inflammation (C‐Reactive Protein, Fibrinogen, proinflammatory cytokines) and energy metabolic status (BMI, leptin, oxidative stress) according to clinical parameters in 104 ovarian cancer patients at different stage and, moreover, to evaluate prospectively the changes of these parameters in accordance to tumour response in a subgroup of 70 advanced stage ovarian cancer patients. Advanced stage and poor PS were associated to high‐grade inflammation and impaired energy metabolism. Among inflammatory mediators, interleukin (IL)‐6 had a central role as predictive factor of leptin, reactive oxygen species and glutathione peroxidase. In turn, leptin considered the key marker of the nutritional status and energy metabolism, was independently determined from stage and IL‐6, not only from BMI. Moreover, the evaluation of the changes of these parameters during the course of the neoplastic disease in the subgroup of advanced ovarian cancer patients clearly unveils the central role of IL‐6 and leptin as early markers of the metabolic alterations and symptoms associated to disease progression in advanced stage ovarian cancer. Their assessment should be included in monitoring disease outcome, especially when cancer is no longer curable and quality of life becomes the primary endpoint.