bluuebunny/crossref_metadata_2025_split huggingface dataset:
The cost of health professionals' brain drain in Kenya
Authors: Kirigia Joses Muthuri , Gbary Akpa Raphael , Muthuri Lenity Kainyu , Nyoni Jennifer , Seddoh Anthony 
Published: July 2006

Abstract
Background
Past attempts to estimate the cost of migration were limited to education costs only and did not include the lost returns from investment. The objectives of this study were: (i) to estimate the financial cost of emigration of Kenyan doctors to the United Kingdom (UK) and the United States of America (USA); (ii) to estimate the financial cost of emigration of nurses to seven OECD countries (Canada, Denmark, Finland, Ireland, Portugal, UK, USA); and (iii) to describe other losses from brain drain.

Methods
The costs of primary, secondary, medical and nursing schools were estimated in 2005. The cost information used in this study was obtained from one non-profit primary and secondary school and one public university in Kenya. The cost estimates represent unsubsidized cost. The loss incurred by Kenya through emigration was obtained by compounding the cost of educating a medical doctor and a nurse over the period between the average age of emigration (30 years) and the age of retirement (62 years) in recipient countries.

Results
The total cost of educating a single medical doctor from primary school to university is US$ 65,997; and for every doctor who emigrates, a country loses about US$ 517,931 worth of returns from investment. The total cost of educating one nurse from primary school to college of health sciences is US$ 43,180; and for every nurse that emigrates, a country loses about US$ 338,868 worth of returns from investment.

Conclusion
Developed countries continue to deprive Kenya of millions of dollars worth of investments embodied in her human resources for health. If the current trend of poaching of scarce human resources for health (and other professionals) from Kenya is not curtailed, the chances of achieving the Millennium Development Goals would remain bleak. Such continued plunder of investments embodied in human resources contributes to further underdevelopment of Kenya and to keeping a majority of her people in the vicious circle of ill-health and poverty. Therefore, both developed and developing countries need to urgently develop and implement strategies for addressing the health human resource crisis.
Detection of estrogen receptors ER-alpha and ER-beta in human ejaculated immature spermatozoa with excess residual cytoplasm
Authors: Rago Vittoria , Siciliano Laura , Aquila Saveria , Carpino Amalia 
Published: July 2006

AbstractBackgroundA key role of estrogens in human sperm biology has been recently suggested by aromatase and estrogen receptor detection in human testicular germ cells and ejaculated spermatozoa. However, the involvement of these hormones in the sperm maturation process is still not defined. The aim of this work was to investigate the expression of estrogen receptors, ER-alpha and ER-beta, in human ejaculated immature spermatozoa with excess residual cytoplasm.MethodsImmunofluorescence labelling has been used to localize ER-alpha and ER-beta proteins in immature spermatozoa isolated by Percoll gradient, while Western blot analysis was carried out on sperm protein extracts.ResultsBoth estrogen receptors were localized in excess residual cytoplasm of immature sperm, while sperm tails showed only ER-beta. Furthermore, in the same cells, immunoblots detected the presence of the full-length (~67 kDa) ER-alpha and (~59 kDa) ER-beta proteins, together with a ~50 kDa ER-beta species, lacking in mature sperm.ConclusionThe present investigation demonstrated ER-alpha and ER-beta presence in excess residual cytoplasm of human abnormal sperm cells, suggesting the hypothesis that both the 'classical' ERs could be able to mediate estrogen action in spermatogenetic cells. Furthermore, the presence of the short ER-beta form in abnormal germ cells and its disappearance in mature sperm, support estrogen modulation via different ER forms during sperm maturation.
Haemostasis, inflammation and renal function following exercise in patients with intermittent claudication on statin and aspirin therapy
Authors: Collins Patrick , Ford Isobel , Croal Bernard , Ball Derek , Greaves Michael , Macaulay Ewan , Brittenden Julie 
Published: July 2006

Abstract

Background
Previous studies have suggested that exercise in patients with intermittent claudication (IC) may induce a systemic thrombo-inflammatory response. The effect of secondary prevention therapy on this response is unknown. This study aimed to investigate the effects of treadmill exercise on markers of coagulation activation, inflammation and renal function in patients with IC, receiving aspirin and statin therapy compared to healthy controls.

Methods
Samples were taken before, immediately and 1 hour after exercising on a treadmill in 20 patients with IC and 20 healthy volunteers. Interleukin-6 (IL-6), thrombin-anti-thrombin complex (TAT) and fibrin D-dimer were measured by ELISA. High sensitivity CRP (HsCRP) and urinary albumin were measured via a nephelometric technique, urinary protein via a turbidometric assay and N-acetyl-β-D-glucosaminidase (NAG) via a colorimetric assay.

Results
Elevated baseline levels of Hs-CRP, IL-6, white cell counts, D-dimer and urinary NAG occurred in patients with IC compared to volunteers (p > 0.05). Following exercise there was no increase in Hs CRP or IL-6. D-dimer levels significantly increased following exercise in the patients and volunteers. TAT levels increased immediately after exercise in the patient group only and were significantly increased at 1 hour in both patients and volunteers. A transient rise in the protein creatinine ratio occurred in both groups (p < 0.007), and in albumin creatinine ratio in the patient group. There was no change in urinary NAG.

Conclusion
Elevated markers of inflammation occurred in patients with IC on statin and aspirin therapy but these did not increase following exercise. However, acute exercise resulted in a prothrombotic state evident in both groups, although this was more prolonged in patient with IC. The clinical significance of these findings in patients who are known to be at an increased risk of cardiac and other thrombotic event are unclear.
The neighborhood food environment: sources of historical data on retail food stores
Authors: Wang May C , Gonzalez Alma A , Ritchie Lorrene D , Winkleby Marilyn A 
Published: July 2006

Abstract
With the rapidly increasing prevalence of obesity in the United States, and the minimal success of education-based interventions, there is growing interest in understanding the role of the neighborhood food environment in determining dietary behavior. This study, as part of a larger study, identifies historical data on retail food stores, evaluates strengths and limitations of the data for research, and assesses the comparability of historical retail food store data from a government and a commercial source.
Five government and commercial listings of retail food stores were identified. The California State Board of Equalization (SBOE) database was selected and then compared to telephone business directory listings. The Spearman's correlation coefficient was used to assess the congruency of food store counts per census tract between the SBOE and telephone business directory databases. The setting was four cities in Northern California, 1979–1990.
The SBOE and telephone business directory databases listed 127 and 351 retail food stores, respectively. The SBOE listed 36 stores not listed by the telephone business directories, while the telephone business directories listed 260 stores not listed by the SBOE. Spearman's correlation coefficients between estimates of stores per census tract made from the SBOE listings and those made from the telephone business directory listings were approximately 0.5 (p < .0001) for the types of stores studied (chain supermarkets, small grocery stores, and chain convenience markets). We conclude that, depending on the specific aims of the study, caution and considerable effort must be exercised in using and applying historical data on retail food stores.
Genetic Polymorphisms in Monoamine Neurotransmitter Systems Show Only Weak Association with Acute Post-Surgical Pain in Humans
Authors: Kim Hyungsuk , Lee Hyewon , Rowan Janet , Brahim Jaime , Dionne Raymond A 
Published: July 2006

Background Candidate gene studies on the basis of biological hypotheses have been a practical approach to identify relevant genetic variation in complex traits. Based on previous reports and the roles in pain pathways, we have examined the effects of variations of loci in the genes of monoamine neurotransmitter systems including metabolizing enzymes, receptors and transporters on acute clinical pain responses in humans. Results Variations in the catecholamine metabolizing enzyme genes ( MAOA and COMT) showed significant associations with the maximum post-operative pain rating while the serotonin transporter gene ( SLC6A4) showed association with the onset time of post-operative pain. Analgesic onset time after medication was significantly associated with the norepinephrine transporter gene ( SLC6A2). However, the association between COMT genetic variation and pain sensitivity in our study differ from previous studies with small sample sizes, population stratification and pain phenotype derived from combining different types of pain stimuli. Correcting for multiple comparisons did not sustain these genetic associations between monoamine neurotransmitter systems and pain sensitivity even in this large and homogeneous sample. Conclusion These results suggest that the previously reported associations between genetic polymorphisms in the monoamine neurotransmitter systems and the interindividual variability in pain responses cannot be replicated in a clinically relevant pain phenotype.
Mastitis and related management factors in certified organic dairy herds in Sweden
Authors: Hamilton Cecilia , Emanuelson Ulf , Forslund Kristina , Hansson Ingrid , Ekman Torkel 
Published: July 2006

Abstract

Background
Mastitis is one of the major threats to animal health, in organic farming as well as conventional. Preliminary studies of organic dairy herds have indicated better udder health in such herds, as compared to conventional herds. The aim of this paper was to further study mastitis and management related factors in certified organic dairy herds.

Methods
An observational study of 26 certified organic dairy herds in mid-eastern Sweden was conducted during one year. A large-animal practitioner visited the herds three times and clinically examined and sampled cows, and collected information about general health and management routines. Data on milk production and disorders treated by a veterinarian in the 26 herds, as well as in 1102 conventional herds, were retrieved from official records. Multivariable logistic regression was used to assess associations between herd type (organic vs. conventional) and incidence of disorders.

Results
The organic herds that took part in the study ranged in size from 12 to 64 cows, in milk production from 3772 to 10334 kg per cow and year, and in bulk milk somatic cell counts from 83000 to 280000 cells/ml. The organic herds were found to have a lower incidence of clinical mastitis, teat injuries, and a lower proportion of cows with a high somatic cell count (as indicated by the UDS, Udder Disease Score) compared to conventional herds. The spectrum of udder pathogenic bacteria was similar to that found in other Swedish studies. Treatment of mastitis was found to be similar to what is practised in conventional herds. Homeopathic remedies were not widely used in the treatment of clinical mastitis.
The calves in most of these organic herds suckled their dams for only a few days, which were not considered to substantially affect the udder health. The main management factor that was different from conventional herds was the feeding strategy, where organic herds used a larger share of forage.

Conclusion
Udder health in Swedish organic herds appears to be better than in conventional herds of comparable size and production. The major difference in management between the two types of farms is the proportion of concentrates fed. The mechanisms explaining the association between intensity of feeding and udder health in dairy cows require further research.
Differential expression, function and response to inflammatory stimuli of 11β-hydroxysteroid dehydrogenase type 1 in human fibroblasts: a mechanism for tissue-specific regulation of inflammation
Authors: Hardy Rowan S , Filer Andrew , Cooper Mark S , Parsonage Greg , Raza Karim , Hardie Debbie L , Rabbitt Elizabeth H , Stewart Paul M , Buckley Christopher D , Hewison Martin 
Published: July 2006

AbstractStromal cells such as fibroblasts play an important role in defining tissue-specific responses during the resolution of inflammation. We hypothesized that this involves tissue-specific regulation of glucocorticoids, mediated via differential regulation of the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Expression, activity and function of 11β-HSD1 was assessed in matched fibroblasts derived from various tissues (synovium, bone marrow and skin) obtained from patients with rheumatoid arthritis or osteoarthritis. 11β-HSD1 was expressed in fibroblasts from all tissues but mRNA levels and enzyme activity were higher in synovial fibroblasts (2-fold and 13-fold higher mRNA levels in dermal and synovial fibroblasts, respectively, relative to bone marrow). Expression and activity of the enzyme increased in all fibroblasts following treatment with tumour necrosis factor-α or IL-1β (bone marrow: 8-fold and 37-fold, respectively, compared to vehicle; dermal fibroblasts: 4-fold and 14-fold; synovial fibroblasts: 7-fold and 31-fold; all P < 0.01 compared with vehicle). Treatment with IL-4 or interferon-γ was without effect, and there was no difference in 11β-HSD1 expression between fibroblasts (from any site) obtained from patients with rheumatoid arthritis or osteoarthritis. In the presence of 100 nmol/l cortisone, IL-6 production – a characteristic feature of synovial derived fibroblasts – was significantly reduced in synovial but not dermal or bone marrow fibroblasts. This was prevented by co-treatment with an 11β-HSD inhibitor, emphasizing the potential for autocrine activation of glucocorticoids in synovial fibroblasts. These data indicate that differences in fibroblast-derived glucocorticoid production (via the enzyme 11β-HSD1) between cells from distinct anatomical locations may play a key role in the predeliction of certain tissues to develop persistent inflammation.
Association of FCGR2A and FCGR2A-FCGR3Ahaplotypes with susceptibility to giant cell arteritis
Authors: Morgan Ann W , Robinson Jim I , Barrett Jennifer H , Martin Javier , Walker Amy , Babbage Sarah J , Ollier William ER , Gonzalez-Gay Miguel A , Isaacs John D 
Published: July 2006

AbstractThe Fc gamma receptors have been shown to play important roles in the initiation and regulation of many immunological and inflammatory processes and to amplify and refine the immune response to an infection. We have investigated the hypothesis that polymorphism within the FCGR genetic locus is associated with giant cell arteritis (GCA). Biallelic polymorphisms in FCGR2A, FCGR3A, FCGR3B and FCGR2B were examined for association with biopsy-proven GCA (n = 85) and healthy ethnically matched controls (n = 132) in a well-characterised cohort from Lugo, Spain. Haplotype frequencies and linkage disequilibrium (D') were estimated across the FCGR locus and a model-free analysis performed to determine association with GCA. There was a significant association between FCGR2A-131RR homozygosity (odds ratio (OR) 2.10, 95% confidence interval (CI) 1.12 to 3.77, P = 0.02, compared with all others) and carriage of FCGR3A-158F (OR 3.09, 95% CI 1.10 to 8.64, P = 0.03, compared with non-carriers) with susceptibility to GCA. FCGR haplotypes were examined to refine the extent of the association. The haplotype showing the strongest association with GCA susceptibility was the FCGR2A-FCGR3A 131R-158F haplotype (OR 2.84, P = 0.01 for homozygotes compared with all others). There was evidence of a multiplicative joint effect between homozygosity for FCGR2A-131R and HLA-DRB1*04 positivity, consistent with both of these two genetic factors contributing to the risk of disease. The risk of GCA in HLA-DRB1*04 positive individuals homozygous for the FCGR2A-131R allele is increased almost six-fold compared with those with other FCGR2A genotypes who are HLA-DRB1*04 negative. We have demonstrated that FCGR2A may contribute to the 'susceptibility' of GCA in this Spanish population. The increased association observed with a FCGR2A-FCGR3A haplotype suggests the presence of additional genetic polymorphisms in linkage disequilibrium with this haplotype that may contribute to disease susceptibility. These findings may ultimately provide new insights into disease pathogenesis.
Coexpression and interaction of CXCL10 and CD26 in mesenchymal cells by synergising inflammatory cytokines: CXCL8 and CXCL10 are discriminative markers for autoimmune arthropathies
Authors: Proost Paul , Struyf Sofie , Loos Tamara , Gouwy Mieke , Schutyser Evemie , Conings René , Ronsse Isabelle , Parmentier Marc , Grillet Bernard , Opdenakker Ghislain , Balzarini Jan , Van Damme Jo 
Published: July 2006

AbstractLeukocyte infiltration during acute and chronic inflammation is regulated by exogenous and endogenous factors, including cytokines, chemokines and proteases. Stimulation of fibroblasts and human microvascular endothelial cells with the inflammatory cytokines interleukin-1β (IL-1β) or tumour necrosis factor alpha (TNF-α) combined with either interferon-α (IFN-α), IFN-β or IFN-γ resulted in a synergistic induction of the CXC chemokine CXCL10, but not of the neutrophil chemoattractant CXCL8. In contrast, simultaneous stimulation with different IFN types did not result in a synergistic CXCL10 protein induction. Purification of natural CXCL10 from the conditioned medium of fibroblasts led to the isolation of CD26/dipeptidyl peptidase IV-processed CXCL10 missing two NH2-terminal residues. In contrast to intact CXCL10, NH2-terminally truncated CXCL10(3–77) did not induce extracellular signal-regulated kinase 1/2 or Akt/protein kinase B phosphorylation in CXC chemokine receptor 3-transfected cells. Together with the expression of CXCL10, the expression of membrane-bound CD26/dipeptidyl peptidase IV was also upregulated in fibroblasts by IFN-γ, by IFN-γ plus IL-1β or by IFN-γ plus TNF-α. This provides a negative feedback for CXCL10-dependent chemotaxis of activated T cells and natural killer cells. Since TNF-α and IL-1β are implicated in arthritis, synovial concentrations of CXCL8 and CXCL10 were compared in patients suffering from crystal arthritis, ankylosing spondylitis, psoriatic arthritis and rheumatoid arthritis. All three groups of autoimmune arthritis patients (ankylosing spondylitis, psoriatic arthritis and rheumatoid arthritis) had significantly increased synovial CXCL10 levels compared with crystal arthritis patients. In contrast, compared with crystal arthritis, only rheumatoid arthritis patients, and not ankylosing spondylitis or psoriatic arthritis patients, had significantly higher synovial CXCL8 concentrations. Synovial concentrations of the neutrophil chemoattractant CXCL8 may therefore be useful to discriminate between autoimmune arthritis types.
Hormone-related risk factors for breast cancer in women under age 50 years by estrogen and progesterone receptor status: results from a case–control and a case–case comparison
Authors: Ma Huiyan , Bernstein Leslie , Ross Ronald K , Ursin Giske 
Published: July 2006

Abstract
Introduction
It has been suggested that hormonal risk factors act predominantly on estrogen receptor and progesterone receptor (ER/PR)-positive breast cancers. However, the data have been inconsistent, especially in younger women.

Methods
We evaluated the impact of age at menarche, pregnancy history, duration of breastfeeding, body mass index, combined oral contraceptive use, and alcohol consumption on breast cancer risk by ER/PR status in 1,725 population-based case patients and 440 control subjects aged 20 to 49 years identified within neighborhoods of case patients. We used multivariable unconditional logistic regression methods to conduct case–control comparisons overall as well as by ER/PR status of the cases, and to compare ER+PR+ with ER-PR- case patients.

Results
The number of full-term pregnancies was inversely associated with the risk of ER+PR+ breast cancer (ptrend = 0.005), whereas recent average alcohol consumption was associated with an increased risk of ER+PR+ breast cancer (ptrend = 0.03). Neither of these two factors was associated with the risk of ER- PR- breast cancer. Late age at menarche and a longer duration of breastfeeding were both associated with decreased breast cancer risk, irrespective of receptor status (all ptrend≤ 0.03).

Conclusion
Our results suggest that the number of full-term pregnancies and recent alcohol consumption affect breast cancer risk in younger women predominantly through estrogen and progesterone mediated by their respective receptors. Late age at menarche and breastfeeding may act through different hormonal mechanisms.
Intrinsic molecular signature of breast cancer in a population-based cohort of 412 patients
Authors: Calza Stefano , Hall Per , Auer Gert , Bjöhle Judith , Klaar Sigrid , Kronenwett Ulrike , Liu Edison T , Miller Lance , Ploner Alexander , Smeds Johanna , Bergh Jonas , Pawitan Yudi 
Published: July 2006

Abstract
Background
Molecular markers and the rich biological information they contain have great potential for cancer diagnosis, prognostication and therapy prediction. So far, however, they have not superseded routine histopathology and staging criteria, partly because the few studies performed on molecular subtyping have had little validation and limited clinical characterization.

Methods
We obtained gene expression and clinical data for 412 breast cancers obtained from population-based cohorts of patients from Stockholm and Uppsala, Sweden. Using the intrinsic set of approximately 500 genes derived in the Norway/Stanford breast cancer data, we validated the existence of five molecular subtypes – basal-like, ERBB2, luminal A/B and normal-like – and characterized these subtypes extensively with the use of conventional clinical variables.

Results
We found an overall 77.5% concordance between the centroid prediction of the Swedish cohort by using the Norway/Stanford signature and the k-means clustering performed internally within the Swedish cohort. The highest rate of discordant assignments occurred between the luminal A and luminal B subtypes and between the luminal B and ERBB2 subtypes. The subtypes varied significantly in terms of grade (p < 0.001), p53 mutation (p < 0.001) and genomic instability (p = 0.01), but surprisingly there was little difference in lymph-node metastasis (p = 0.31). Furthermore, current users of hormone-replacement therapy were strikingly over-represented in the normal-like subgroup (p < 0.001). Separate analyses of the patients who received endocrine therapy and those who did not receive any adjuvant therapy supported the previous hypothesis that the basal-like subtype responded to adjuvant treatment, whereas the ERBB2 and luminal B subtypes were poor responders.

Conclusion
We found that the intrinsic molecular subtypes of breast cancer are broadly present in a diverse collection of patients from a population-based cohort in Sweden. The intrinsic gene set, originally selected to reveal stable tumor characteristics, was shown to have a strong correlation with progression-related properties such as grade, p53 mutation and genomic instability.