bluuebunny/crossref_metadata_2025_split huggingface dataset:
Families on the Move: The Changing Role of Afghan Refugee Women in Iran
Authors: Hoodfar Homa 
Published: July 2004

AbstractIn their attempts to "modernize" and bring about socio-economic change, Afghan governments have been preoccupied with restructuring the institutions of marriage and family, and women's role within them, since the 1880s. Serious commitment to introduce legal reform and democratize the family and gender roles cost King Amanullah his throne (1919–1929). From 1930 to 1976 the government attempted a gradual approach introducing reforms piecemeal which had little impact beyond the capital and major cities. After the coup d'état in 1973 and the installation of socialism, the regime introduced a new family decree (known as Number 7) in October 1978 and aggressively pursued women's education and the reform of family laws. This policy incensed the conservative communities and tribal societies, who rebelled against the government; the ensuing Russian occupation brought about the resistance movements and subsequent civil war that has wreaked havoc on Afghanistan for more than two decades. Many conservatives who had tried to resist the intended changes regarding family law and education for girls and "protect" their women, who represented the males honor, decided to leave the country with their families. More than six million Afghans moved to neighboring countries, mostly to Iran and Pakistan. Examining data collected among Afghan refugees in Iran from 1999 to 2002, this paper argues that, ironically, living in exile has brought about the very changes resistance to which had forced them into the refugee situation. Forced to cope with a crisis situation, they developed economic and social survival strategies that altered women's role. Moreover, that exposure to an Islamic society very different from their own brought about structural and ideological changes in the family and in gender roles which legal reforms in Afghanistan had failed to induce. Given the considerable size of the refugee population in Iran (but also in Pakistan and elsewhere) and the destruction of the old fabric(s) of Afghan society, this paper argues that these changes may be irreversible.
Interleukin-15 enhances immune reconstitution after allogeneic bone marrow transplantation
Authors: Alpdogan Onder , Eng Jeffrey M. , Muriglan Stephanie J. , Willis Lucy M. , Hubbard Vanessa M. , Tjoe Kartono H. , Terwey Theis H. , Kochman Adam , van den Brink Marcel R. M. 
Published: July 2004

AbstractInterleukin-15 (IL-15) is a γ-common cytokine that plays an important role in the development, survival, and proliferation of natural killer (NK), NK T, and CD8+ T-cells. We administered IL-15 to recipients of an allogeneic bone marrow transplantation (allo BMT) to determine its effects on immune reconstitution. Posttransplantation IL-15 administration significantly increased donor-derived CD8+ T (mostly CD122+CD44+CD8+ T-cells), NK, and NK T-cells at day +28 in young and old recipients of allo BMT. This was associated with enhanced T-cell and NK-cell function. IL-15 stimulated homeostatic proliferation of donor CD8+ T-cells in recipients of carboxyfluorescein diacetate succinimidyl ester–labeled donor T-cell infusions. Posttransplantation IL-15 administration also resulted in a decrease in apoptotic CD8+ T-cells, an increase in Bcl-2–expressing CD8+ T-cells, and an increase in the fraction of Ki67+ proliferative NK and CD8+ T-cells in recipients of allo BMT. IL-15 did not exacerbate graft-versus-host disease (GVHD) in recipients of T-cell–depleted BMT but could aggravate GVHD in some cases in recipients of a T-cell–repleted BMT. Finally, we found that IL-15 administration could enhance graft-versus-leukemia activity. In conclusion, IL-15 can be administered safely to recipients of a T-cell–depleted allo BMT to enhance CD8+ T, NK, and NK T-cell reconstitution.
Surface fucosylation of human cord blood cells augments binding to P-selectin and E-selectin and enhances engraftment in bone marrow
Authors: Xia Lijun , McDaniel J. Michael , Yago Tadayuki , Doeden Andrea , McEver Rodger P. 
Published: July 2004

AbstractMurine hematopoietic stem and progenitor cells (HSPCs) home to bone marrow in part by rolling on P-selectin and E-selectin expressed on endothelial cells. Human adult CD34+ cells, which are enriched in HSPCs, roll on endothelial selectins in bone marrow vessels of nonobese diabetic/severe combined immune deficiency (NOD/SCID) mice. Many human umbilical cord blood (CB) CD34+ cells do not roll in these vessels, in part because of an uncharacterized defect in binding to P-selectin. Selectin ligands must be α1-3 fucosylated to form glycan determinants such as sialyl Lewis x (sLex). We found that inadequate α1-3 fucosylation of CB CD34+ cells, particularly CD34+CD38–/low cells that are highly enriched in HSPCs, caused them to bind poorly to E-selectin as well as to P-selectin. Treatment of CB CD34+ cells with guanosine diphosphate (GDP) fucose and exogenous α1-3 fucosyltransferase VI increased cell-surface sLex determinants, augmented binding to fluid-phase P- and E-selectin, and improved cell rolling on P- and E-selectin under flow. Similar treatment of CB mononuclear cells enhanced engraftment of human hematopoietic cells in bone marrows of irradiated NOD/SCID mice. These observations suggest that α1-3 fucosylation of CB cells might be a simple and effective method to improve hematopoietic cell homing to and engraftment in bone marrows of patients receiving CB transplants.
Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation
Authors: Min Chang-Ki , Maeda Yoshinobu , Lowler Kathleen , Liu Chen , Clouthier Shawn , Lofthus David , Weisiger Elizabeth , Ferrara James L. M. , Reddy Pavan 
Published: July 2004

AbstractAdministration of exogenous interleukin-18 (IL-18) regulates experimental acute graft-versus-host disease (GVHD) in a Fas-dependent manner when donor CD4+ T cells are required for mortality after experimental allogeneic bone marrow transplantation (BMT). However, CD4+ and CD8+ T cells can induce acute GVHD after clinical allogeneic BMT, and the role of IL-18 in CD8+-mediated acute GVHD is unknown. We, therefore, determined the role of IL-18 in GVHD mediated by CD4+ or CD8+ T cells across major histocompatibility complex (MHC) class II- and class I-disparate allogeneic BMT, respectively. Administering IL-18 significantly increased survival in CD4+-mediated GVHD but reduced survival in CD8+-mediated GVHD. This increase in deaths was associated with significantly greater clinical, biochemical, and histopathologic parameters of GVHD damage and was independent of Fas expression on donor T cells. Administering IL-18 significantly enhanced allospecific cytotoxic function and expansion of CD8+ cells. Endogenous IL-18 was critical to GVHD mediated by CD8+ donor T cells because IL-18 receptor-deficient donors caused significantly less GVHD but exacerbated CD4+-mediated, GVHD-related death. Furthermore, administering anti-IL-18 monoclonal antibody significantly reduced CD8+-mediated, GVHD-related death. Together these findings demonstrate that IL-18 has paradoxical effects on CD4+ and CD8+ cell-mediated GVHD. (Blood. 2004;104:3393-3399)
G6PD is indispensable for erythropoiesis after the embryonic-adult hemoglobin switch
Authors: Paglialunga Francesca , Fico Annalisa , Iaccarino Ingram , Notaro Rosario , Luzzatto Lucio , Martini Giuseppe , Filosa Stefania 
Published: July 2004

AbstractGlucose 6-phosphate dehydrogenase (G6PD) (EC 1.1.1.42) is an essential enzyme for the rapid production of NADPH, as required on exposure to oxidative stress. Mouse embryonic stem (ES) cells can produce all embryonic and fetal/adult cell types. By studying the in vitro differentiation of embryoid bodies produced from G6pdΔ ES cells that are totally unable to produce G6PD protein, we found that these cells are able to differentiate into mesodermal cells, cardiomyocytes, hepatocytes, and primitive erythroid cells. However, we show here that, after the hemoglobin switch has taken place, definitive erythrocytes die by apoptosis. This apoptotic death is delayed by reducing agents and by a caspase inhibitor, but it is prevented only by the restoration of G6PD activity. Thus, G6PD proves indispensable for definitive erythropoiesis.
Megakaryocyte proliferation and ploidy regulated by the cytoplasmic tail of glycoprotein Ibα
Authors: Kanaji Taisuke , Russell Susan , Cunningham Janet , Izuhara Kenji , Fox Joan E. B. , Ware Jerry 
Published: July 2004

AbstractWe have investigated the ability of glycoprotein (GP) Ibα, a megakaryocytic gene product, to sequester the signal transduction protein 14-3-3ξ and to influence megakaryocytopoiesis. Using a Gp1ba–/– mouse colony, we compared the rescued phenotypes produced by a wild-type human GP Ibα allele or a similar allele containing a 6-residue cytoplasmic tail truncation that abrogates binding to 14-3-3ξ. The observed phenotypes illustrate an involvement for GP Ibα in thrombopoietin-mediated events of megakaryocyte proliferation, polyploidization, and the expression of apoptotic markers in maturing megakaryocytes. We developed a hypothesis for the involvement of a GP Ibα/14-3-3ξ/PI-3 kinase complex in regulating thrombopoietin-mediated responses. An observed increase in thrombopoietin-mediated Akt phosphorylation in the truncated variant supported the hypothesis and led to the development of a model in which the GP Ibα cytoplasmic tail sequestered signaling proteins during megakaryocytopoiesis and, as such, became a critical regulator in the temporal sequence of events that led to normal megakaryocyte maturation.
Mouse CD99 participates in T-cell recruitment into inflamed skin
Authors: Bixel Gabriele , Kloep Stephan , Butz Stefan , Petri Björn , Engelhardt Britta , Vestweber Dietmar 
Published: July 2004

AbstractHuman CD99 is a small highly O-glycosylated cell-surface protein expressed on most leukocytes. It was recently found to be expressed at endothelial cell contacts and to participate in the transendothelial migration (TEM) of monocytes in vitro. In order to analyze the physiologic relevance of CD99 in vivo we searched for the mouse homolog. We cloned a mouse cDNA coding for a protein 45% identical in its sequence with human CD99. Based on the cDNA, we generated antibodies against this mouse homolog of CD99, which detected the antigen on most leukocytes, on endothelia of various tissues, and at cell contacts of cultured endothelial cells. Cell aggregation of CD99-transfected Chinese hamster ovary (CHO) cells was completely blocked by anti-CD99 antibodies. The same antibodies inhibited TEM of lymphocytes in vitro, independent of whether T cells or endothelial cells were preincubated with antibodies. In a cutaneous delayed-type hypersensitivity (DTH) reaction, anti-CD99 antibodies inhibited the recruitment of in vivo–activated T cells into inflamed skin as well as edema formation. We conclude that mouse CD99 participates in the TEM of lymphocytes and in their recruitment to inflamed skin in vivo. This establishes CD99 as a valid target for interference with cutaneous inflammatory processes.
PDGF-D induces macrophage recruitment, increased interstitial pressure, and blood vessel maturation during angiogenesis
Authors: Uutela Marko , Wirzenius Maria , Paavonen Karri , Rajantie Iiro , He Yulong , Karpanen Terhi , Lohela Marja , Wiig Helge , Salven Petri , Pajusola Katri , Eriksson Ulf , Alitalo Kari 
Published: July 2004

Abstract
Platelet-derived growth factor-D (PDGF-D) is a recently characterized member of the PDGF family with unknown in vivo functions. We investigated the effects of PDGF-D in transgenic mice by expressing it in basal epidermal cells and then analyzed skin histology, interstitial fluid pressure, and wound healing. When compared with control mice, PDGF-D transgenic mice displayed increased numbers of macrophages and elevated interstitial fluid pressure in the dermis. Wound healing in the transgenic mice was characterized by increased cell density and enhanced recruitment of macrophages. Macrophage recruitment was also the characteristic response when PDGF-D was expressed in skeletal muscle or ear by an adeno-associated virus vector. Combined expression of PDGF-D with vascular endothelial growth factor-E (VEGF-E) led to increased pericyte/smooth muscle cell coating of the VEGF-E–induced vessels and inhibition of the vascular leakiness that accompanies VEGF-E–induced angiogenesis. These results show that full-length PDGF-D is activated in tissues and is capable of increasing interstitial fluid pressure and macrophage recruitment and the maturation of blood vessels in angiogenic processes.
Long-term acquisition of allergen-specific IgE and asthma following allogeneic bone marrow transplantation from allergic donors
Authors: Hallstrand Teal S. , Sprenger Jay D. , Agosti Jan M. , Longton Gary M. , Witherspoon Robert P. , Henderson William R. 
Published: July 2004

Abstract
Adoptive transfer of allergen-specific immunoglobulin E (IgE) from atopic donors to nonatopic recipients occurs during the first year following bone marrow transplantation (BMT). Mature B- and T-cell clones with allergen-specific memory and hematopoietic progenitor cells are transferred through BMT. The objective of this study was to characterize the long-term rate of allergic sensitization and development of clinical allergic diseases following BMT from atopic donors. A long-term follow-up study was conducted in a cohort of donor and recipient pairs with moderate-to-severe allergic disease in the donor prior to BMT. Assessments of allergen-specific IgE, clinical rhinitis, and asthma were made in the donors prior to BMT and in the recipients with a mean follow-up of 15.5 years after BMT. From an initial cohort of 12 bone marrow transplant recipients who received marrow from allergic donors, 5 long-term survivors were identified. Allergen-specific IgE transferred from donor to recipient following BMT frequently persisted, and a high rate of de novo allergic sensitization was observed between 1 and 14 years after BMT. These events were associated with elevation in total IgE, and development of allergic rhinitis and asthma at long-term follow-up. We conclude that marrow-derived immune cells from allergic donors can transfer the predisposition to allergy and asthma.
New strategies to improve exercise tolerance in chronic obstructive pulmonary disease
Authors: Ambrosino N. , Strambi S. 
Published: July 2004

Breathlessness is the most common symptom limiting exercise in patients with chronic obstructive pulmonary disease (COPD). Exercise training can improve both exercise tolerance and health status in these patients, intensity being of key importance. Nevertheless, in these patients extreme breathlessness and/or peripheral muscle fatigue may prevent patients from higher levels of intensity. In this review article the literature concerning the different ways to optimise exercise tolerance in patients with COPD, with the objective of enhancing the tolerance to higher exercise training intensity, is summarised.Continuous positive airway pressure and different modalities of noninvasive positive pressure ventilation (NPPV) may reduce breathlessness and increase exercise tolerance in these patients. Respiratory muscle unloading and reduction in intrinsic positive end-expiratory pressure have been considered among mechanisms underlying these effects. Nevertheless, the role of NPPV in pulmonary rehabilitation, if any, is still controversial. The addition of nocturnal domiciliary NPPV during a daily exercise programme in patients with severe COPD resulted in an improvement in exercise tolerance and quality of life.In patients with severe COPD application of electrical stimulation combined with active limb mobilisation significantly improved muscle strength, and interval training has been shown capable of inducing physiological training effects.Oxygen supplementation in patients who do not desaturate during exercise seems to be the most promising treatment, since it allows for higher exercise intensities and, therefore, superior training efficacy.In conclusion, further studies are needed to define the appropriate patients in order to generalise such interventions. The modalities discussed should be used as adjuncts to a well designed comprehensive respiratory rehabilitation programme.
Sarcoidosis and granuloma genes: a family-based study in African-Americans
Authors: Rybicki B.A. , Maliarik M.J. , Poisson L.M. , Iannuzzi M.C. 
Published: July 2004

The evidence for a genetic component in the aetiology of sarcoidosis includes familial aggregation, associations with genetic polymorphisms, and linkage to the major histocompatibility complex class region on chromosome 6p. Unfortunately, the majority of genetic associations with sarcoidosis have not been consistently replicated.In the present study, using a family-based study design, which controls for population stratification, the authors attempted to replicate previously reported associations between sarcoidosis and three attractive candidate genes studied primarily in case-control samples.In 225 nuclear families, ascertained through African Americans with a history of sarcoidosis, no evidence was found for an association between sarcoidosis susceptibility and polymorphisms in the angiotensin converting enzyme, vitamin D receptor and tumour necrosis factor‐α genes. Further analyses of chronic and acute disease phenotypes failed to reveal any notable associations. Assuming an underlying inheritance model with an additive allelic effect on disease risk, the current study had ∼80–90% statistical power to detect a 3‐fold increased risk associated with the putative risk allele of the polymorphisms under study.The present authors conclude that in African-Americans, the angiotensin converting enzyme, vitamin D receptor, and tumour necrosis factor‐α genes are not significant risk factors for sarcoidosis susceptibility.
Dyspnoea at rest and at the end of different exercises in patients with near-fatal asthma
Authors: Barreiro E. , Gea J. , Sanjuás C. , Marcos R. , Broquetas J. , Milic-Emili J. 
Published: July 2004

Blunted perception of dyspnoea under resistive loading has been observed in patients with a history of near-fatal asthma (NFA). The perception of dyspnoea at rest and at the end point of various exercises was assessed in such patients.Respiratory function and exercise capacity (6‐min walking distance, incremental cycloergometry and inspiratory threshold loading) were assessed in seven NFA and eight non-NFA patients. Dyspnoea (Borg scale) was measured at rest and at the end point of the various exercises.Dyspnoea at rest was significantly lower in NFA patients. Although exercise tolerance was similarly reduced in both the NFA and non-NFA groups, dyspnoea at peak cycle exercise was significantly lower in the former (2.6±2versus6.1±3.8 (Borg scale; mean±sd)), who mainly (86%) stopped because of leg discomfort. A similar trend was observed in the 6‐min walking distance and inspiratory threshold loading tests. Dyspnoea at peak exercise was the best indicator of the NFA condition, with a sensitivity of 100% and specificity of 63% for a Borg scale score of ≤6.Perception of dyspnoea is blunted in near-fatal asthma patients at both rest and the end point of various forms of exercise. Dyspnoea at peak exercise is the best indicator of the near-fatal asthma condition.
Performance vigilance task and sleepiness in patients with sleep-disordered breathing
Authors: Sforza E. , Haba-Rubio J. , De Bilbao F. , Rochat T. , Ibanez V. 
Published: July 2004

Altered vigilance performance has been documented in patients with sleep-related breathing disorders (SRBDs). Sleep fragmentation, sleepiness, respiratory disturbances and nocturnal hypoxaemia have been suggested as the pathogenesis of these deficits, yet it remains difficult to find a good correlation between performance deficits and the above factors. In the present study, which performance measure better characterised SRBD patients and the main factors implicated in these disturbances were examined.The study group consisted of 152 patients and 45 controls, all examined using a performance vigilance task and subjective sleepiness assessment. Speed and accuracy in the psychomotor vigilance task (PVT) were measured in patients and controls. Objective daytime sleepiness was assessed in the patient group using the maintenance of wakefulness test.In comparison with controls, PVT accuracy rather than speed seems to be affected in SRBD patients, with lapses and false responses significantly greater in patients with more severe objective sleepiness and higher apnoea/hypopnoea index. Although slowing and increased variability in reaction time were associated with shorter sleep latency in the maintenance of wakefulness test, subjective sleepiness, sleep fragmentation, nocturnal hypoxaemia and apnoea/hypopnoea index influenced mainly PVT accuracy.It is concluded that vigilance impairment, sleep fragmentation and severity of disease may partially and differentially contribute to the diurnal performance consequences found in sleep-related breathing disorders. Since the psychomotor vigilance task worsening is more marked in accuracy that in speed, measurement of lapses and false responses would better characterise the degree of diurnal impairment in these patients.
Airway iron and iron-regulatory cytokines in cystic fibrosis
Authors: Reid D.W. , Lam Q.T. , Schneider H. , Walters E.H. 
Published: July 2004

Iron availability is critical toPseudomonas aeruginosa. The current authors determined sputum iron, ferritin, microalbumin levels and total cell counts (TCC) in 19 adult patients with cystic fibrosis (CF) during an acute exacerbation and repeated analyses following a median of 12 days antibiotic treatment. The current authors also determined sputum interleukin (IL)‐1β and tumour necrosis factor (TNF)‐α levels because of their putative role in intracellular iron homeostasis. Additional data were obtained from 17 stable CF patients, eight patients with stable chronic obstructive pulmonary disease (COPD) and six normal subjects.Overall, sputum iron, ferritin, microalbumin, IL‐1β and TNF‐α concentrations and TCCs were significantly elevated in the CF patients compared to those with COPD and normal controls. Sputum ferritin levels were significantly elevated in acuteversusstable CF patients and there was a trend for sputum TCC to be higher, but all other inflammatory indices were similar. In the CF patients, sputum iron was positively and strongly related to IL‐1β, TNF‐α, ferritin and microalbumin levels, but negatively related to forced expiratory volume in one second % predicted. In those acute patients who clinically improved with antibiotics (n=14), there were significant decreases in sputum TCC, iron, ferritin and IL‐1β content, but not TNF‐α or albumin levels. However, changes in sputum TNF‐α in acute patients were still closely related to changes in iron, ferritin and albumin content, and changes in IL‐1β were related to changes in sputum ferritin content.Iron and iron-regulatory cytokines may play a role in cystic fibrosis lung disease and the increased iron content may even facilitatePseudomonas aeruginosainfection.