bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantitiative Analysis of Roughness of Catheters by Scanning Electron Microscopy (SEM) and Atomic Force Microscopy (AFM).
Authors: Chan Anthony , Parmar Nagina , Jega Anusha , Yip Christopher , Farrokhyar Forough , Walton Mark J. 
Published: October 2019

Abstract
Thrombosis is a major complication of central venous access devices, and incidence depends on material, diameter, tip position, and tip surface. Catheters are usually cut to the appropriate length for accurate positioning. However, cutting is not recommended as rough surfaces can serve as a nidus for thrombi. This study was done to assess the roughness of the catheter tips as provided by various manufacturers, versus the roughness once cut and handled. Four types of catheters (Groschong, Hickman, Port-a-Cath, and Per Q Cath) were cut by scissors, iris scissors, or scalpel, and handled with debakey forceps, a needle driver, and adsons with or without teeth, to determine the damage created on the catheter. The manufactured tip was compared as a control. Scanning electron microscopy (SEM) was used to do imaging for all samples and roughness and section analysis was quantified using atomic force microscopy (AFM) for the cutting methods. SEM showed that scalpel-cut and manufactured ends appeared smoother relative to those cut with scissors or iris scissors (Fig 1). This complemented the roughness and section analysis by AFM (Fig 2). Catheters handled by debakey equipment and adsons with teeth showed the most roughness, visible as deep holes or a grainy surface when observed by high magnification SEM. Decreasing smoothness of catheters is in the following order: uncut surface, followed by surfaces cut by scalpel, scissors or iris scissors. Handling should be minimized and use of adsons with teeth, needle drivers and debakey forceps avoided, which can leave permanent damage. The least damage appeared to be adsons without teeth. Thus, the cutting of catheters is not recommended since rough surfaces can serve as a thrombotic nidus.
Figure Figure
The Effect of beta-Thalassemia Minor on the Optic Nerve Head Analysis.
Authors: Cetin Turker , Mutlu Fatih M. , Avcu Ferit , Mumcuoglu Tarkan , Nevruz Oral , Ural Ali U. 
Published: October 2019

Abstract
Background: A variety of ophthalmologic findings have been reported in patients with anemia.
Aim: To determine the effect of beta-thalassemia minor on the optic nerve head topographic analysis.
Methods: A total of 39 beta-thalassemia minor patients were divided into 2 groups. Patients with iron, folic acid, or vitamin B12 deficiency were ruled out. Group 1 comprised 20 patients with anemia, and group 2 comprised 19 patients without anemia. One eye of each patient was included into the study. All subjects underwent complete ocular examination. Optic nerve head topographic analysis was performed by using a confocal scanning laser ophthalmoscope type Heidelberg retina tomograph (HRT). The following stereometric parameters were evaluated: disc area, area and volume of cup, area and volume of neuroretinal rim, measure of cup shape, and mean retinal nerve fiber layer thickness.
Results: The mean age of group 1 and 2 were 26.8±7.6 and 25.6±4.5 years, respectively (P=0.91). Their mean disc areas were 2.01±0.3 mm2 and 2.53±0.6 mm2, respectively (P =0.009). The differences between groups for area and volume of cup, area and volume of neuroretinal rim, cup shape measure, and mean retinal nerve fiber layer thickness were insignificant (p>0.05). There was no significant difference between mean intraocular pressure of both groups (p=0.93).
Conclusion: In beta-thalassemia minor, patients with anemia, optic disc area showed a statistically significant reduction compared to the patients without anemia. Further clinical trials on ocular blood flow and optic nerve oxygenation changes may highlight the role anemia in the optic nerve head of the beta-thalassemia minor patients.
Correlation between Entothelial Microparticle Binding to Monocytes and Monocyte Nitric Oxide Production in Prothrombotic and Inflammatory Disorders.
Authors: Chirinos Julio A. , Jy Wenche , Del Carpio Freddy , Arteaga Roque , Gustavo Heresi A. , Valvidia Martin , Horstman Lawrence L. , Jimenez Joaquin J. , Ahn Yeon S. 
Published: October 2019

Abstract
Introduction: Endothelial microparticle binding to monocytes has been shown to induce monocyte activation in vitro. In this study, we examined the correlations between EMP binding to monocytes and monocyte levels of nitric oxide (NO), as a marker of monocyte activation in different clinical conditions.
Methods: We studied 186 subjects with acute venous thromboembolism (n=25), atrial fibrillation (n=48), metabolic syndrome (n=37), congestive heart failure (n=44), and normal controls (n=32). Using flow cytometry, we measured monocyte levels of NO by flow cytometry after loading monocytes with the membrane permeable NO-selective fluorescent indicator DAF-DA. Two different populations of EMP-monocyte conjugates were also measured. EMP62E+-monocyte and EMP54+-monocyte conjugates were measured based on the detection of E-selectin (CD62E) or CD54, respectively, coexpressed with CD45 in monocytes.
Results: Pearson correlation coefficients between monocyte NO levels and EMP-monocyte conjugates are shown in the Table. A highly significant correlation was found between EMP62E+-monocyte conjugates and monocyte NO levels in patients with congestive heart failure (r=0.43; p=0.003). In contrast, EMP54+-monocyte conjugates strongly correlated with monocyte NO in patients with venous thromboembolism (r=0.58; p=0.009) and metabolic syndrome (r=0.49; p=0.002). No correlation was found between these conjugates and monocyte NO levels in atrial fibrillation or normal controls.
Conclusions: The binding of different species of EMP to monocytes correlates with monocyte NO levels in clinical states such as congestive heart failure, metabolic syndrome, and venous thromboembolism. However, this correlation was not found in atrial fibrillation or normal controls. Our findings support the concept that the binding of different species of EMP exert different biological effects and/or reflect different biologic processes in specific disease states. Further research is needed to determine whether the binding of EMP species to monocytes regulates nitric oxide production by monocytes and whether monocytes themselves regulate the binding of different species of EMP in different disease states.
Correlation between Monocyte NO levels and EMP-Monocyte Conjugates in different conditions. EMP54+-Monocyte Conjugates EMP62E+-Monocyte Conjugates Pearson r p value Pearson r p value Metabolic Syndrome 0.49 0.002 0.13 0.54 Venous Thromboembolism 0.51 0.009 0.12 0.57 Congestive Heart Failure 0.22 0.14 0.43 0.003 Atrial Fibrillation 0.22 0.14 0.17 0.24 Normal Controls 0.03 0.85 0.27 0.13
Tumor Necrosis Factor-a Enhances Human Leukemia Cell Differentiation Induced by DMSO, but Not Retinoic Acid.
Authors: Yu Hong-Nu , Lee Young-Rae , Shim Hyun-Jaung , Han Myung-Kwan , Song Eun-Kyung , Park Jinny , Kim Jong-Suk 
Published: October 2019

Abstract
One of the human leukemia treatment methods is to differentiate leukemia cells into mature cells. Because differentiated cells lose their proliferative and tumor-forming abilities, differentiation inducers may be useful for the treatment of leukemia. Differentiation of leukemia cells has been studied using HL60 cells, a human promyelocytic leukemia cell line, which can be differentiated into granulocyte-like or monocyte/macrophage-like cells by various pharmacological agents such as dimethyl sulfoxide (DMSO), retinoic acid and phorbol myristic acetate (PMA). We previously reported that nuclear factor - kB (NF-kB) activation plays the important role in DMSO-induced differentiation of HL60 cells. Thus, we hypothesized that NF-kB activators could enhance DMSO-induced differentiation of HL60 cells. Here we examine whether tumor necrosis factor-a (TNF-a), a potent NF-kB inducer, enhance DMSO-induced differentiation of HL60 cells. TNF-a was found to enhance HL60 cell differentiation induced by DMSO. CD11b, a differentiation marker, was increased in 0.5 % DMSO-treated cells compared to control cells. When TNF-a was added to the same condition, CD11b expression was further enhanced in a dose and a time dependent manners. We also found that nitro blue tetrazolium (NBT) reducing activity, a marker for granulocytic differentiation, was further increased in DMSO plus TNF-a treated cells compared to only DMSO- treated cells. However, TNF-a alone had no effect on CD11b expression and NBT reducing activity. The enhancement of DMSO-induced HL60 differentiation by TNF-a was offset by NF-kB inhibition. Interestingly, retinoic acid- induced differentiation of HL60 cells showed no enhancing effect of TNF--a on the differentiation. These findings indicate that TNF--a might affect only NF-kB dependent differentation of HL60 cells. Taken together, we demonstrated that TNF-a enhances DMSO-induced differentiation of HL60 cells by stimulating NF-kB activation. Our results suggest that NF-kB inducers such as TNF-a are useful for the treatment of leukemia in combination with DMSO.
Sub-Marginal Endothelial Cells Dynamically Regulate Endothelial Sheet Migration.
Authors: Ofori-Acquah Solomon F. 
Published: October 2019

Abstract
Migration of endothelial cells as a sheet in fully differentiated blood vessels is essential for reducing vascular permeability during wound healing. Indeed, loss of collective endothelial sheet migration contributes to increased vascular permeability in tumor angiogenesis and several vascular proliferative disorders. Despite this significance, mechanisms responsible for keeping migrating endothelial cells in a monolayer, sheet or tube are poorly understood. To unravel the basis for collective endothelial cell migration, we used time-lapse video microscopy to study early events of wound closure in confluent monolayers of primary microvascular endothelial cells in a live cell chamber. Immediately after wounding (0– 20 min), endothelial cells at the margin of the wound (marginal cells) retracted away from the wounded area and showed no visible lamellipodia extensions. The next phase of early wound healing (20 min – 6 hours) revealed extensive lamellipodia formation and migration of marginal cells into the wounded region. Remarkably, sub-marginal endothelial cells that were several microns away from the wound edge protruded lamellipodia that formed dynamic cell-cell contacts with the substratum of marginal cells at the wound edge. In several instances sub-marginal cells physically and coordinately pulled back endothelial cells at wound edge to maintain regularity of the endothelial sheet front. Cell-tracking measurements revealed autonomous and yet coordinated migration of marginal and sub-marginal endothelial cells culminating in net protrusion of the endothelial sheet into the wound. This study provides in real-time evidence of retraction of endothelial cells at the wound edge by several microns prior to the initiation of forward migration. In addition, we show for the first time that endothelial cells several microns away from the wound edge actively participate in sheet migration through the extention of lamellipodia into the substratum of cells at the wound edge. These findings highlight an important role in endothelial sheet migration for the Rho family of GTPases given their intimate control of cell retraction and lamelipodia extensions. Future studies will directly evaluate the influence of Rac, Cdc42 and RhoA in retraction of marginal cells and formation of lamellipodia by sub-marginal cells in endothelial sheet migration.
NIH-Funded Research Using Human Embryonic Stem Cells.
Authors: Blau C. Anthony , Nelson Angelique , Ware Carol B. 
Published: October 2019

Abstract
In October 2003, the National Institutes of Health (NIH) established three extramural “Exploratory Centers for Human Embryonic Stem Cell Research.” Our Center’s experience in acquiring and manipulating NIH-approved human embryonic stem (hES) cell lines may be useful for other institutions interested in pursuing NIH-funded hES cell research. We acquired 14 of the 22 NIH-approved cell lines. Modifications to the proposed Material Transfer Agreements (MTAs) with hES cell suppliers were sought to improve accessibility to these hES cell lines by local researchers. Lines were characterized for survival following cryopreservation and for their ability to adapt to a uniform set of culture conditions while maintaining a normal karyotype. Each of the 4 suppliers contacted eventually agreed to terms that improved access to their hES cell lines. Eleven hES cell lines were received frozen, and in 10 cases very few cells survived cryopreservation. Ten hES cell lines were successfully converted to simplified culture conditions that enhanced their ability to be maintained and expanded in culture. One hES cell line had an unstable karyotype at an early passage. Current MTA provisions continue to present significant obstacles to NIH-funded hES cell research. Many hES cell lines can be maintained using culture conditions less onerous than those recommended by their suppliers.
The South East England Thrombotic Thrombocytopenic Purpura Registry.
Authors: Scully Marie , Yarranton Helen , Liesner Ri , Cavenagh Jamie , Hunt Beverley , Benjamin Sylvia , Laffan Michael , Bevan David , Mackie Ian , Machin Samuel J. 
Published: October 2019

Abstract
Thrombotic thrombocytopenic purpura (TTP) is an acute, rare, life threatening disorder. We present data from the South East (SE) England registry for TTP, from April 2002–December 2005. Included are 156 patients and 179 acute episodes. Seventy four percent of cases were female and 26% males, median age at presentation, 41 and 47.5 years respectively. Mortality to December 2003 was 12%, and from January 2004 to December 2005 was 5%; 5/12 died before treatment was instigated. The main ethnic groups were Caucasian (63%), Afro Caribbean (22%) and Asian (12%). In 61%, this was their first TTP episode; 39% represented with acute relapse. Precipitating events (n=123); idiopathic (56%), a defined infection (11%), pregnancy (6%), HIV disease (7%), congenital (5%) and associated autoimmune disease (6%). Features at presentation include: neurological disease (39%), temperature (15%), abdominal symptoms (12%), renal impairment (10%), symptomatic cardiac disease (7%), symptoms related to low platelets (17%) and no symptoms (2%). From April 2002–December 2003, the median number of plasma exchanges until complete remission (CR) recorded in 36 patients was 20 (5–79). One patient received plasma infusion (PI) in conjunction with PEX. 33 patients received 3 doses of pulsed intravenous methylprednisolone (IV MP) and 9 orally. Other therapies used were Rituximab (1), defibrotide (5), cyclosporine (9) and vincristine (15). In the second cohort (January 2004–December 2005), the median number of PEX to CR in 88 episodes was 8 (3–80). PI was used in 5 cases, 48 patients received 3 doses of pulsed IV MP on admission and 6 patients oral prednisolone. Other therapies used were Rituximab (26), defibrotide (2), cyclosporine (3), vincristine (5) and BPL 8Y (9). The latter is an intermediate purity Factor VIII concentrate used in congenital TTP. The median Haemoglobin (Hb) was 9.9g/dL at presentation and platelet count 18 ×109/L. The 2002–2003 group had 48% cases with platelet counts <150 ×109/L at 7 days, but only 25% of cases in 2004–2005. ADAMTS 13 activity, measured by collagen binding assay (CBA) (normal range 66–126%), in 136 episodes was <5% in 60%, 5–40% in 21%, 40–66 in 12% and >66% in 7% at presentation. Antibody to ADAMTS 13 (determined by mixing studies using CBA and/or anti-ADAMTS 13 IgG antibodies) was present in 61% of all cases. In those patients with acute idiopathic TTP, 93% had associated antibody. In conclusion: Improved recognition and prompt diagnosis of TTP may be associated with reduction in mortality and changes in treatment protocols reduced the number of PEX to achieve CR. Acute idiopathic TTP is the most common presentation, but improved identification of subgroups such as HIV and congenital TTP have resulted in appropriate tailoring of therapy.
TDAG51 Deficiency Promotes Migration and Proliferation of Mouse Embryonic Fibroblasts.
Authors: Hossain Gazi S. , Dickhout Jeffrey G. , McCulloch Christopher A. , Zhou Ji , May Linda , Al-Bayati Hiam , Rho J. , Austin Richard C. 
Published: October 2019

Abstract
T-cell death associated gene 51 (TDAG51) is a member of the pleckstrin homology-related domain family having pro-apoptotic characteristics. Indirect immunofluorescence studies demonstrate that endogenous TDAG51 co-localizes with focal adhesion kinase (FAK), a molecule found within focal adhesion complexes (FACs). FACs are believed to be the structural connection between the extracellular matrix (ECM) and actin cytoskeleton. Given that overexpression of TDAG51 promotes detachment-induced programmed cell death (PCD) and that TDAG51 co-localizes with FAK, it was proposed that deficiency of TDAG51 may stabilize FAC assembly, thereby affecting actin cytoskeletal organization and/or cell migration. To better understand the role of TDAG51 in cell migration, mouse embryonic fibroblasts (MEFs) deficient in TDAG51 were derived from TDAG51-deficient mice and compared to wild type MEFs. TDAG51-deficient MEFs showed increased migration following monolayer disruption or in response to chemotaxis on fibronectin-coated Boyden Chambers. In addition, loss of TDAG51 promotes the proliferation of MEFs. Collagen gel contraction experiments were performed to confirm the aggregate effect of the differences in migration and proliferation observed in TDAG51-deficient MEFs. Interestingly, migration and proliferation can be blocked by active b-integrin inhibitory antibody. In terms of a cellular phenotype, migratory TDAG51-deficient MEFs have distinct filopodial and lamellipodial extentions, compared to migratory wild type MEFs. Laser scanning confocal microscope demonstrated a significant decrease in F-actin stress fibers as well as increased distribution of vinculin within the lamellipodial protrusions of TDAG51-deficient MEFs. Importantly, reintroduction of TDAG51 into TDAG51-deficient MEFs reversed these phenotypic changes. Taken together, our findings suggest that loss of TDAG51 affects cell migration and proliferation through modifying focal adhesion complex assembly and cytoskeletal rearrangements.
Clinical Usefulness of the Simple Technique To Diagnose Thrombocytopenia Using Immature Platelet Fraction (IPF).
Authors: Cho Yong Gon , Lee Jae Hyun , Kim Dal Sik , Lee Hye Soo , Choi Sam Im 
Published: October 2019

Abstract
Background : It is defined that immature platelet fraction (IPF) is the percentage of reticulated platelet (RP) of total platelet count. We have measured an IPF reference range using XE-2100 blood cell counter with upgraded software (Sysmex, Kobe, Japan) and evaluated the clinical utility of this parameter for the laboratory diagnosis of thrombocytopenia due to increased peripheral platelet destruction.
Materials and methods : Peripheral blood samples collected into K2EDTA (Beckton Dickinson, Franklin Lakes, NJ, USA) were analysed at Chonbuk National University Hospital. 142 samples from apparently healthy adults (all routine full blood count parameters including platelets within the healthy reference range) were used to establish a normal reference range for the IPF%. The patients are classified 3 group including hypoplastic (consisted of 22 patients undergoing chemotherapy with falling platelet counts and 14 with aplastic anemia), destructive (14 with ITP and 7 with infection), and cirrhotic (40 with cirrhosis of liver).
Results : An IPF reference range in healthy individuals was established as 0.4~5.4%, with a mean of 1.7%. The significant increase in IPF values was found in destructive patient group. The cut-off value of IPF is 6.0%, its sensitivity and specificity are 95.2%, 82.9% respectively. Reproducibility was good.
Conclusion : A rapid, inexpensive automated method for measuring the IPF% is feasible and should become a standard parameter in evaluating the thrombocytopenic patient.
Use of Activated Recombinant Factor VII for the Control of Post Partum Hemorrhage (PPH).
Authors: Hossain Nazli H. , Farzana Tasneem F. , Shamsi Tahir S. , Soomro Nargis S. 
Published: October 2019

Abstract
Objective: To evaluate the efficacy and safety of activated recombinant factor VII (rFVIIa) in the control of PPH
Patients and Methods: All patients with massive PPH who failed medical and surgical treatment were eligible for the investigation. Massive PPH was defined as loss of > 1000 ml of blood within 24 h after delivery. Patients were considered for treatment with rFVIIa after failure of conventional measures such administration of myotonic agents including oxytocin, ergotamine, misoprostol and failure of other interventions aimed at controlling blood loss such as ligation of uterine and ovarian vessels, or ligation of internal iliac artery. The primary outcome measures were control of the bleeding episode and reduction in the number of administered blood products.
Results: A total of 16 patients with massive PPH were eligible for the current study. Vaginal and vacuum delivery was used in 6 patients while 10 patients underwent C-section. The mean dose of rFVIIa was 68 mcg/kg administered intravenously as a single bolus injection. Mean time of diagnosing PPH and administration was 5.5 hours (+/−2). The mean number of blood products used prior the administration of rFVIIa was 14 units RBC and 12 units of FFP. Cessation of blood loss was achieved in 14 patients within an average of 20 minutes after the administration of rFVIIa. The blood products utlilized after the administration of rFVIIa in these patients were 2 URBC and 2UFFP. The uterus was conserved in 7 patients who received rFVIIa prior to hysterectomy. While in 9 patients rFVIIa was administered after failure of hysterectomy to control blood loss. Of the 16 patients, 3 died because of multiorgan failure following severe blood loss. No adverse events including thromboembolic phenomena were observed.
Conclusion: Massive PPH is the most common cause of maternal mortality in developing countries. The use of rFVIIa in patients with massive PPH can achieve hemostasis with a single dose only. The administration of rFVIIa in patients with massive PPH may avoid the need for hysterectomy. There were no safety issues in the current study. Further trials should address the dose and timing of administration of rFVIIa in patients with massive PPH.