bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ex vivo expansion of human hematopoietic stem and progenitor cells
Authors: Dahlberg Ann , Delaney Colleen , Bernstein Irwin D. 
Published: March 2011

AbstractDespite progress in our understanding of the growth factors that support the progressive maturation of the various cell lineages of the hematopoietic system, less is known about factors that govern the self-renewal of hematopoietic stem and progenitor cells (HSPCs), and our ability to expand human HSPC numbers ex vivo remains limited. Interest in stem cell expansion has been heightened by the increasing importance of HSCs in the treatment of both malignant and nonmalignant diseases, as well as their use in gene therapy. To date, most attempts to ex vivo expand HSPCs have used hematopoietic growth factors but have not achieved clinically relevant effects. More recent approaches, including our studies in which activation of the Notch signaling pathway has enabled a clinically relevant ex vivo expansion of HSPCs, have led to renewed interest in this arena. Here we briefly review early attempts at ex vivo expansion by cytokine stimulation followed by an examination of our studies investigating the role of Notch signaling in HSPC self-renewal. We will also review other recently developed approaches for ex vivo expansion, primarily focused on the more extensively studied cord blood–derived stem cell. Finally, we discuss some of the challenges still facing this field.
HIV disease progression despite suppression of viral replication is associated with exhaustion of lymphopoiesis
Authors: Sauce Delphine , Larsen Martin , Fastenackels Solène , Pauchard Michèle , Ait-Mohand Hocine , Schneider Luminita , Guihot Amélie , Boufassa Faroudy , Zaunders John , Iguertsira Malika , Bailey Michelle , Gorochov Guy , Duvivier Claudine , Carcelain Guislaine , Kelleher Anthony D. , Simon Anne , Meyer Laurence , Costagliola Dominique , Deeks Steven G. , Lambotte Olivier , Autran Brigitte , Hunt Peter W. , Katlama Christine , Appay Victor 
Published: March 2011

AbstractThe mechanisms of CD4+ T-cell count decline, the hallmark of HIV disease progression, and its relationship to elevated levels of immune activation are not fully understood. Massive depletion of CD4+ T cells occurs during the course of HIV-1 infection, so that maintenance of adequate CD4+ T-cell levels probably depends primarily on the capacity to renew depleted lymphocytes, that is, the lymphopoiesis. We performed here a comprehensive study of quantitative and qualitative attributes of CD34+ hematopoietic progenitor cells directly from the blood of a large set of HIV-infected persons compared with uninfected donors, in particular the elderly. Our analyses underline a marked impairment of primary immune resources with the failure to maintain adequate lymphocyte counts. Systemic immune activation emerges as a major correlate of altered lymphopoiesis, which can be partially reversed with prolonged antiretroviral therapy. Importantly, HIV disease progression despite elite control of HIV replication or virologic success on antiretroviral treatment is associated with persistent damage to the lymphopoietic system or exhaustion of lymphopoiesis. These findings highlight the importance of primary hematopoietic resources in HIV pathogenesis and the response to antiretroviral treatments.
Evaluation of the impact of the voucher and accreditation approach on improving reproductive health behaviors and status in Kenya
Authors: Warren Charlotte , Abuya Timothy , Obare Francis , Sunday Joseph , Njue Rebecca , Askew Ian , Bellows Ben 
Published: March 2011

Abtsract

Background
Alternatives to the traditional 'supply-side' approach to financing service delivery are being explored. These strategies are termed results-based finance, demand-side health financing or output-based aid which includes a range of interventions that channel government or donor subsidies to the user rather than the provider. Initial pilot assessments of reproductive health voucher programs suggest that, they can increase access and use, reducing inequities and enhancing program efficiency and service quality. However, there is a paucity of evidence describing how the programs function in different settings, for various reproductive health services. Population Council, funded by the Bill and Melinda Gates Foundation, intends to generate evidence around the 'voucher and accreditation' approaches to improving the reproductive health of low income women in Kenya.

Methods/Design
A quasi-experimental study will investigate the impact of the voucher approach on improving reproductive health behaviors, reproductive health status and reducing inequities at the population level; and assessing the effect of vouchers on increasing access to, and quality of, and reducing inequities in the use of selected reproductive health services. The study comprises of four populations: facilities, providers, women of reproductive health age using facilities and women and men who have been pregnant and/or used family planning within the previous 12 months. The study will be carried out in samples of health facilities - public, private and faith-based in: three districts; Kisumu, Kiambu, Kitui and two informal settlements in Nairobi which are accredited to provide maternal and newborn health and family planning services to women holding vouchers for the services; and compared with a matched sample of non-accredited facilities. Health facility assessments (HFA) will be conducted at two stages to track temporal changes in quality of care and utilization. Facility inventories, structured observations, and client exit interviews will be used to collect comparable data across facilities. Health providers will also be interviewed and observed providing care. A population survey of about 3000 respondents will also be carried out in areas where vouchers are distributed and similar locations where vouchers are not distributed.
The quality of reporting of primary test accuracy studies in obstetrics and gynaecology: application of the STARD criteria
Authors: Selman Tara J , Morris R Katie , Zamora Javier , Khan Khalid S 
Published: March 2011

Abstract

Background
In obstetrics and gynaecology there has been a rapid growth in the development of new tests and primary studies of their accuracy. It is imperative that such studies are reported with transparency allowing the detection of any potential bias that may invalidate the results. The objective of this study was to determine the quality of reporting in diagnostic test accuracy studies in obstetrics and gynaecology using the Standards for Reporting of Diagnostic Accuracy - STARD checklist.

Methods
The included studies of ten systematic reviews were assessed for compliance with each of the reporting criteria. Using appropriate statistical tests we investigated whether there was an improvement in reporting quality since the introduction of the STARD checklist, whether a correlation existed between study sample size, country of origin of study and reporting quality.

Results
A total of 300 studies were included (195 for obstetrics, 105 for gynaecology). The overall reporting quality of included studies to the STARD criteria was poor. Obstetric studies reported adequately > 50% of the time for 62.1% (18/29) of the items while gynaecologic studies did the same 51.7% (15/29). There was a greater mean compliance with STARD criteria in the included obstetric studies than the gynaecological (p < 0.0001). There was a positive correlation, in both obstetrics (p < 0.0001) and gynaecology (p = 0.0123), between study sample size and reporting quality. No correlation between geographical area of publication and compliance with the reporting criteria could be demonstrated.

Conclusions
The reporting quality of papers in obstetrics and gynaecology is improving. This may be due to initiatives such as the STARD checklist as well as historical progress in awareness among authors of the need to accurately report studies. There is however considerable scope for further improvement.
Helicobacter pylori phagosome maturation in primary human macrophages
Authors: Borlace Glenn N , Jones Hilary F , Keep Stacey J , Butler Ross N , Brooks Doug A 
Published: March 2011

Abstract

Background

Helicobacter pylori (H. pylori) is a micro-aerophilic, spiral-shaped, motile bacterium that is the principal cause of gastric and duodenal ulcers in humans and is a major risk factor for the development of gastric cancer. Despite provoking a strong innate and adaptive immune response in the host, H. pylori persists in the gastric mucosa, avoiding eradication by macrophages and other phagocytic cells, which are recruited to the site of infection. Here we have characterised the critical degradative process of phagosome maturation in primary human macrophages for five genotypically and phenotypically distinct clinical strains of H. pylori.

Results
All of the H. pylori strains examined showed some disruption to the phagosome maturation process, when compared to control E. coli. The early endosome marker EEA1 and late endosome marker Rab7 were retained on H. pylori phagosomes, while the late endosome-lysosome markers CD63, LAMP-1 and LAMP-2 were acquired in an apparently normal manner. Acquisition of EEA1 by H. pylori phagosomes appeared to occur by two distinct, strain specific modes. H. pylori strains that were negative for the cancer associated virulence factor CagA were detected in phagosomes that recruited large amounts of EEA1 relative to Rab5, compared to CagA positive strains. There were also strain specific differences in the timing of Rab7 acquisition which correlated with differences in the rate of intracellular trafficking of phagosomes and the timing of megasome formation. Megasomes were observed for all of the H. pylori strains examined.

Conclusions

H. pylori appeared to disrupt the normal process of phagosome maturation in primary human macrophages, appearing to block endosome fission. This resulted in the formation of a hybrid phagosome-endosome-lysosome compartment, which we propose has reduced degradative capacity. Reduced killing by phagocytes is consistent with the persistence of H. pylori in the host, and would contribute to the chronic stimulation of the inflammatory immune response, which underlies H. pylori-associated disease.
Processing of Proaugurin Is Required to Suppress Proliferation of Tumor Cell Lines
Authors: Ozawa Akihiko , Lick Adam N. , Lindberg Iris 
Published: March 2011

AbstractAugurin is a secretory molecule produced in pituitary, thyroid, and esophagus and implicated in a wide array of physiological processes, from ACTH release to tumor suppression. However, the specific proaugurin-derived peptides present in various cell types are not yet known. In order to shed light on the posttranslational modifications required for biological activity, we here describe the posttranslational processing of proaugurin in AtT-20 and Lovo cells and identify proaugurin-derived products generated by convertases. In vitro cleavage of proaugurin with proprotein convertases produced multiple peptides, including a major product with a mass of 9.7 kDa by mass spectrometry. Metabolic labeling of C-terminally tagged proaugurin in AtT-20 and AtT-20/PC2 cells resulted in a major 15-kDa tagged form on SDS-PAGE, which likely corresponds to the 9.7-kDa in vitro fragment, with the added tag, its linker, and posttranslational modification(s). The secretion of neither proaugurin nor this cleavage product was stimulated by forskolin, indicating its lack of storage in regulated secretory granules and lack of cleavage by PC2. Incubation of cells with the furin inhibitor nona-d-arginine resulted in impaired cleavage of proaugurin, whereas metalloprotease inhibitors did not affect proaugurin proteolysis. These data support the idea that proaugurin is cleaved by furin and secreted via the constitutive secretory pathway. Interestingly, proaugurin was sulfated during trafficking; sulfation was completely inhibited by brefeldin A. Proliferation assays with three different tumor cell lines demonstrated that only furin-cleaved proaugurin could suppress cell proliferation, suggesting that proteolytic cleavage is a posttranslational requirement for proaugurin to suppress cell proliferation.
Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer
Authors: Lamont Kristin R. , Tindall Donald J. 
Published: March 2011

AbstractAdvanced prostate tumors, which are androgen dependent, are often initially treated in the clinic with hormone ablation therapy, either through surgical castration or administration of small-molecule antiandrogens. Most tumors respond favorably to these treatments, exhibiting regression of the tumor, amelioration of symptoms, and a decrease of prostate-specific antigen in patient sera. However, with time, the majority of tumors recur in a more aggressive, castration-resistant (CR) phenotype. Currently, no effective treatment exists for this stage of the cancer, and patients ultimately succumb to metastatic disease. The androgen receptor (AR), which is a member of the nuclear hormone receptor superfamily of proteins, is the transcription factor that is responsible for mediating the effects of androgens upon target tissues, and it has been demonstrated to play a central role in the development and progression of prostate cancer. Despite CR tumor cells being able to continue to grow after hormonal therapy in which testosterone and dihydrotestosterone are markedly reduced, they still require the expression and activity of the AR. The AR can become transactivated in this low-androgen environment through a number of different mechanisms, including amplification and mutation of the receptor, cross talk with other signaling pathways, and altered regulation by coregulatory proteins. This review will summarize the most current data regarding non-ligand-mediated activation of the AR in prostate cancer cells. Developing work in this field aims to more clearly elucidate the signals that drive AR activity independently of androgens in CR disease so that better therapeutic targets can be developed for patients with this stage of highly aggressive prostate carcinoma.
Identification, tissue distribution and orexigenic activity of neuropeptide F (NPF) in penaeid shrimp
Authors: Christie Andrew E. , Chapline M. Christine , Jackson James M. , Dowda Jenilee K. , Hartline Niko , Malecha Spencer R. , Lenz Petra H. 
Published: March 2011

SUMMARY
The neuropeptide Fs (NPFs) are an invertebrate subgroup of the FMRFamide-like peptides, and are proposed by some to be the homologs of vertebrate neuropeptide Y. Although there is some information about the identity, tissue distribution and function of NPFs in insects, essentially nothing is known about them in crustaceans. We have identified and characterized NPF-encoding transcripts from the penaeid shrimp Litopenaeus vannamei and Melicertus marginatus. Two transcripts were identified from each species. For each shrimp species, the two transcripts differed from one another by the presence or absence of an insert in the portion of the open reading frame that encodes the NPF peptide. The two NPF isoforms are identical in L. vannamei and M. marginatus, with their predicted structures being KPDPSQLANMAEALKYLQELDKYYSQVSRPRFamide and KPDPSQLANMAEALKYLQELDKYYSQVSRPSPRSAPGPASQIQALENTLKFLQLQELGKLYSLRARPRFamide. RT-PCR tissue profiling showed both transcripts are broadly distributed within the nervous system of each species. The transcript encoding the shorter NPF was detected in some, but not all, midgut samples. The transcript encoding the longer NPF was absent in the midgut of both species, and neither transcript was detected in their skeletal muscle. Juvenile L. vannamei fed on a diet supplemented with the shorter NPF exhibited a marked increase in food intake relative to control individuals that did not receive the supplement; the NPF-fed shrimp also showed a significant increase in growth relative to the control group. Our data suggest that NPF is present in both the nervous system and midgut of penaeid shrimp, functioning, at least in part, as a powerful orexigenic agent.
Organization of Functional Synaptic Connections between Medullary Reticulospinal Neurons and Lumbar Descending Commissural Interneurons in the Neonatal Mouse
Authors: Szokol Karolina , Glover Joel C. , Perreault Marie-Claude 
Published: March 2011

The medullary reticular formation (MRF) of the neonatal mouse is organized so that the medial and lateral MRF activate hindlimb and trunk motoneurons (MNs) with differential predominance. The goal of the present study was to investigate whether this activation is polysynaptic and mediated by commissural interneurons with descending axons (dCINs) in the lumbar spinal cord. To this end, we tested the polysynapticity of inputs from the MRF to MNs and tested for the presence of selective inputs from medial and lateral MRF to 574 individual dCINs in the L2 segment of the neonatal mouse.Reticulospinal-mediated postsynaptic Ca2+responses in MNs were reduced in the presence of mephenesin and after a midline lesion, suggesting the involvement of dCINs in mediating the responses. Consistent with this, stimulation of reticulospinal neurons in the medial or lateral MRF activated 51% and 57% of ipsilateral dCINs examined (255 and 352 dCINs, respectively) and 52% and 46% of contralateral dCINs examined (166 and 133 dCINs, respectively). The proportion of dCINs that responded specifically to stimulation of medial or lateral MRF was similar to the proportions of dCINs that responded to both MRF regions or to neither. The three responsive dCIN populations had largely overlapping spatial distributions.We demonstrate the existence of dCIN subpopulations sufficient to mediate responses in lumbar motoneurons from reticulospinal pathways originating from the medial and lateral MRF. Differential control of trunk and hindlimb muscles by the medullary reticulospinal system may therefore be mediated in part by identifiable dCIN populations.
The Role of Keratinized Mucosa in Peri-Implant Health
Authors: Esper Luis Augusto , Ferreira Samuel Barros , de Oliveira Fortes Kaizer Rosane , de Almeida Ana Lúcia Pompéia Fraga 
Published: March 2011

Objective To evaluate the role of keratinized mucosa around dental implants, correlating with other clinical parameters related to the success of dental implants. Design Cross-section. Setting Institutional tertiary referral hospital. Patients A total of 202 dental implants fixed in the cleft area of 109 patients with cleft lip and/or palate were evaluated. Interventions The evaluated clinical parameters were probing depth and gingival and plaque indexes on the buccal surface (three sites). Main Outcome Measures All clinical parameters were correlated with the width of keratinized mucosa around the implants. Results The largest probing depths were detected when the width of keratinized mucosa was 2 mm or more, with a statistically significant difference between the means of the probing depth and keratinized mucosa width. Conclusion Even though the present results suggest that peri-implant health can be observed in areas with keratinized mucosa width under 2 mm provided an adequate oral hygiene control is performed, longitudinal randomized studies are necessary to analyze the relationship between the width of keratinized mucosa and the health of peri-implant tissues.
Evaluation of a 3D Stereophotogrammetric Technique to Measure the Stone Casts of Patients with Unilateral Cleft Lip and Palate
Authors: Sforza Chiarella , De Menezes Marcio , Bresciani Elena , Cerón-Zapata Ana M. , López-Palacio Ana M. , Rodriguez-Ardila Myriam J. , Berrio-Gutiérrez Lina M. 
Published: March 2011

Objective To assess a three-dimensional stereophotogrammetric method for palatal cast digitization of children with unilateral cleft lip and palate. Design As part of a collaboration between the University of Milan (Italy) and the University CES of Medellin (Colombia), 96 palatal cast models obtained from neonatal patients with unilateral cleft lip and palate were obtained and digitized using a three-dimensional stereophotogrammetric imaging system. Main Outcome Measures Three-dimensional measurements (cleft width, depth, length) were made separately for the longer and shorter cleft segments on the digital dental cast surface between landmarks, previously marked. Seven linear measurements were computed. Systematic and random errors between operators' tracings, and accuracy on geometric objects of known size were calculated. In addition, mean measurements from three-dimensional stereophotographs were compared statistically with those from direct anthropometry. Results The three-dimensional method presented good accuracy error (<0.9%) on measuring geometric objects. No systematic errors between operators' measurements were found ( p > .05). Statistically significant differences ( p < 5%) were noted for different methods (caliper versus stereophotogrammetry) for almost all distances analyzed, with mean absolute difference values ranging between 0.22 and 3.41 mm. Therefore, rates for the technical error of measurement and relative error magnitude were scored as moderate for Ag-Am and poor for Ag-Pg and Am-Pm distances. Generally, caliper values were larger than three-dimensional stereophotogrammetric values. Conclusions Three-dimensional stereophotogrammetric systems have some advantages over direct anthropometry, and therefore the method could be sufficiently precise and accurate on palatal cast digitization with unilateral cleft lip and palate. This would be useful for clinical analyses in maxillofacial, plastic, and aesthetic surgery.
Environmental Lead Pollution and Elevated Blood Lead Levels Among Children in a Rural Area of China
Authors: Lin Sihao , Wang Xiaorong , Yu Ignatius Tak Sun , Tang Wenjuan , Miao Jianying , Li Jin , Wu Siying , Lin Xing 
Published: March 2011

Objectives. We investigated environmental lead pollution and its impact on children's blood lead levels (BLLs) in a rural area of China. Methods. In 2007, we studied 379 children younger than 15 years living in 7 villages near lead mines and processing plants, along with a control group of 61 children from another village. We determined their BLLs and collected environmental samples, personal data, and information on other potential exposures. We followed approximately 86% of the children who had high BLLs (> 15 μg/dL) for 1 year. We determined factors influencing BLLs by multivariate linear regression. Results. Lead concentrations in soil and household dust were much higher in polluted villages than in the control village, and more children in the polluted area than in the control village had elevated BLLs (87%, 16.4 μg/dL vs 20%, 7.1 μg/dL). Increased BLL was independently associated with environmental lead levels. We found a significant reduction of 5 micrograms per deciliter when we retested children after 1 year. Conclusions. Our data show that the lead industry caused serious environmental pollution that led to high BLLs in children living nearby.