tbuckley/cabot-search huggingface dataset:
A randomized, double-blind, placebo- and active-controlled, half-head study to evaluate the effects of platelet-rich plasma on alopecia areata
Authors: A. Trink, E. Sorbellini, P. Bezzola, L. Rodella, R. Rezzani, Y. Ramot, F. Rinaldi
Journal: British Journal of Dermatology (2013)

Alopecia areata (AA) is a common autoimmune condition, causing inflammation-induced hair loss. This disease has very limited treatment possibilities, and no treatment is either curative or preventive. Platelet-rich plasma (PRP) has emerged as a new treatment modality in dermatology, and preliminary evidence has suggested that it might have a beneficial role in hair growth.To evaluate the efficacy and safety of PRP for the treatment of AA in a randomized, double-blind, placebo- and active-controlled, half-head, parallel-group study.Forty-five patients with AA were randomized to receive intralesional injections of PRP, triamcinolone acetonide (TrA) or placebo on one half of their scalp. The other half was not treated. Three treatments were given for each patient, with intervals of 1 month. The endpoints were hair regrowth, hair dystrophy as measured by dermoscopy, burning or itching sensation, and cell proliferation as measured by Ki-67 evaluation. Patients were followed for 1 year.PRP was found to increase hair regrowth significantly and to decrease hair dystrophy and burning or itching sensation compared with TrA or placebo. Ki-67 levels, which served as markers for cell proliferation, were significantly higher with PRP. No side-effects were noted during treatment.This pilot study, which is the first to investigate the effects of PRP on AA, suggests that PRP may serve as a safe and effective treatment option in AA, and calls for more extensive controlled studies with this method.
Semaphorin 4F as a Critical Regulator of Neuroepithelial Interactions and a Biomarker of Aggressive Prostate Cancer
Authors: Yi Ding, Dandan He, Diego Florentin, Anna Frolov, Sue Hilsenbeck, Michael Ittmann, Dov Kadmon, Brian Miles, David Rowley, Gustavo Ayala
Journal: Clinical Cancer Research (2013)

Semaphorin 4F (S4F) has roles in embryologic axon guidance and is expressed in adults. S4F is involved in cancer-induced neurogenesis.Prostate cells were transfected with S4F retrovirus. Cells and controls were used for a bromodeoxyuridine (BrdUrd) incorporation assay (proliferation) and in vitro scratch and Matrigel Transwell chamber invasion assay (migration). Monoclonal antibodies were developed using baculovirus-expressed recombinant GST-S4F and used to immunostain tissue microarrays. Slides were imaged using deconvolution and analyzed using tissue segmentation. Data were correlated with clinicopathologic parameters, other biomarkers and survival analysis conducted. Heterogeneity of S4F expression was analyzed with unsupervised clustering algorithms.Proliferation rates measured by BrdUrd incorporation were higher in all S4F-transfected cells. S4F overexpression was associated with increased motility of the cancer cells. S4F expression was overexpressed in high-grade prostatic intraepithelial neoplasia/prostate cancer than normal epithelium. S4F expression correlated with seminal vesicle invasion. Patients with high values of S4F in prostate cancer cytoplasm are at significantly higher risk of biochemical recurrence, by univariate and multivariate analyses. S4F cytoplasmic expression in prostate cancer cells also correlates with nerve density in prostate cancer and perineural invasion diameter. Correlations were identified with NF-κB and inversely with apoptosis in perineural invasion.These data show that S4F is significantly involved in human prostate cancer progression. S4F is a key regulator of the interactions between nerves in the tumor microenvironment and cancer cells. Because of the importance of cancer nerve interaction in the biology of cancer and its clinical implication, S4F can be considered a major therapeutic target. Clin Cancer Res; 19(22); 6101-11. ©2013 AACR.
Divergent evolution of arrested development in the dauer stage of Caenorhabditis elegans and the infective stage of Heterodera glycines
Authors: Axel A Elling, Makedonka Mitreva, Justin Recknor, Xiaowu Gai, John Martin, Thomas R Maier, Jeffrey P McDermott, Tarek Hewezi, David McK Bird, Eric L Davis, Richard S Hussey, Dan Nettleton, James P McCarter, Thomas J Baum
Journal: Genome biology (2007)

Abstract Background The soybean cyst nematode Heterodera glycines is the most important parasite in soybean production worldwide. A comprehensive analysis of large-scale gene expression changes throughout the development of plant-parasitic nematodes has been lacking to date. Results We report an extensive genomic analysis of H. glycines , beginning with the generation of 20,100 expressed sequence tags (ESTs). In-depth analysis of these ESTs plus approximately 1,900 previously published sequences predicted 6,860 unique H. glycines genes and allowed a classification by function using InterProScan. Expression profiling of all 6,860 genes throughout the H. glycines life cycle was undertaken using the Affymetrix Soybean Genome Array GeneChip. Our data sets and results represent a comprehensive resource for molecular studies of H. glycines . Demonstrating the power of this resource, we were able to address whether arrested development in the Caenorhabditis elegans dauer larva and the H. glycines infective second-stage juvenile (J2) exhibits shared gene expression profiles. We determined that the gene expression profiles associated with the C. elegans dauer pathway are not uniformly conserved in H. glycines and that the expression profiles of genes for metabolic enzymes of C. elegans dauer larvae and H. glycines infective J2 are dissimilar. Conclusion Our results indicate that hallmark gene expression patterns and metabolism features are not shared in the developmentally arrested life stages of C. elegans and H. glycines , suggesting that developmental arrest in these two nematode species has undergone more divergent evolution than previously thought and pointing to the need for detailed genomic analyses of individual parasite species.
Risk factors for peptic ulcer disease: a population based prospective cohort study comprising 2416 Danish adults
Authors: S Rosenstock
Journal: Gut (2003)

No population based prospective cohort study has previously assessed the impact of multiple risk factors, including Helicobacter pylori infection, on the incidence of peptic ulcer disease (PUD).To identify risk factors for PUD and estimate their relative impact on ulcer incidence.Random sample of 2416 Danish adults with no history of PU.Sample members were interviewed in 1982 and 1994. PUs diagnosed within the observation period were verified through medical records. Information on psychosocial factors, lifestyle practices, and medication was obtained from a questionnaire completed at study entry. H pylori infection status was determined by ELISA.The main risk factors for PUD were H pylori infection (odds ratio 4.3 (95% confidence interval 2.2; 8.3)), tobacco smoking (3.8 (1.7; 9.8)), and use of minor tranquillisers (3.0 (1.4; 6.6)). Intake of non-steroid anti-inflammatory drugs did not affect the incidence of PUD (0.4 (0.1; 2.3)). In those with increased antibodies to H pylori, tobacco smoking (12.7 (2.8; 56.8)) and intake of spirits (2.4 (1.1; 5.4)) increased the risk of PUD whereas moderate leisure time physical activity (0.3 (0.2; 0.7)) protected against PUD.Tobacco smoking and H pylori infection are the main risk factors for PUD in Danish adults. Physical activity may protect against PUD in those infected with H pylori.
8-Iso-Prostaglandin F <sub>2α</sub> as a Risk Marker in Patients With Coronary Heart Disease
Authors: Cristina Vassalle, Maria Grazia Andreassi
Journal: Circulation (2004)

To the Editor:We read with great interest the manuscript by Schwedhelm et al 1 reporting that urinary levels of 8-iso-prostagladin F 2␣ (8-isoprostane) represent an independent and cumulative risk factor of coronary artery disease (CAD) together with different cardiovascular risk factors.We agree that elevated levels of oxidative stress may be a risk factor for the onset and progression of the atherosclerotic process.However, we would like to draw attention to some assertions in this article.As quoted by the authors, we have recently observed that elevated levels of 8-isoprostane are associated with the extent and severity of CAD and with the occurrence of different atherogenic risk factors. 2 Schwedhelm and colleagues did not find a similar association between 8-isoprostane levels and the severity of CAD.Nevertheless, we measured 8-isoprostane levels in plasma and not in urinary samples, as the authors incorrectly reported.The measurements in different biological samples may account, at least in part, for the differences observed.Differences in population characteristics may also account for the lack of correlation with severity of CAD.In our study, we included patients referred for coronary angiography.Coronary stenosis was considered significant if there was luminal diameter narrowing of Ն50% in at least one epicardial coronary artery.Schwedhelm et al 1 recruited patients who had ischemia symptoms and controls who were asymptomatic for CAD.However, it is not clear whether all patients had undergone coronary angiography.Thus, the authors could clarify this point and inform Circulation readers on which criteria to determine CAD severity were adopted.Finally, the gas chromatography-tandem mass spectrometry (GC/MS) method is extremely reliable but also elaborate, requiring complex instrumentation and specialized operators.This fact likely limits the application of this knowledge for routine clinical diagnosis.Recent results indicate that the evaluation of F(2)isoprostane with enzyme immunoassay (EIA) correlates well with values obtained by the GC/MS method 3 .The use of simple biological markers of oxidative stress may be relevant in adding a new predictive and prognostic factor of CAD.Thus, EIA could represent a straightforward and rapid procedure for evaluating oxidative stress particularly suitable for routine application, because it allows the use of equipment commonly present even in biochemical laboratories.
Bad medicine: using surrogate markers
Authors: S. J. McNulty, P. Williams
Journal: BMJ (2014)

Spence reports that nalmefene has been approved by the Scottish Medicines Consortium (and is being considered by the National Institute for Health and Care Excellence) for alcohol misuse on the basis of criteria such as a reduction in “high drinking levels” and increases in “non-drinking days,” with minimal improvements in liver function tests.1 Although we agree that improvements in liver …
An in vivo study of a growth-factor enhanced, cell free, two-layered collagen–tricalcium phosphate in deep osteochondral defects
Authors: Tobias Gotterbarm, Wiltrud Richter, Martin Jung, Simona Berardi Vilei, Pierre Mainil-Varlet, Takeshi Yamashita, Steffen J. Breusch
Journal: Biomaterials (2006)
Activation of NAD(P)H Oxidase by Tryptophan-Derived 3-Hydroxykynurenine Accelerates Endothelial Apoptosis and Dysfunction In Vivo
Authors: Qiongxin Wang, Miao Zhang, Ye Ding, Qilong Wang, Wencheng Zhang, Ping Song, Ming-Hui Zou
Journal: Circulation Research (2013)

The kynurenine (Kyn) pathway is the major route for tryptophan (Trp) metabolism in mammals. The Trp-Kyn pathway is reported to regulate several fundamental biological processes, including cell death.The aim of this study was to elucidate the contributions and molecular mechanism of Trp-Kyn pathway to endothelial cell death.Endogenous reactive oxygen species, endothelial cell apoptosis, and endothelium-dependent and endothelium-independent vasorelaxation were measured in aortas of wild-type mice or mice deficient for nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase subunits (p47(phox) or gp91(phox)) or indoleamine-pyrrole 2,3-dioxygenase 1 with or without angiotensin (Ang) II infusion. As expected, AngII increased plasma levels of Kyn- and 3-hydroxykynurenine-modified proteins in endothelial cells in vivo. Consistent with this, AngII markedly increased the expression of indoleamine-pyrrole 2,3-dioxygenase in parallel with increased expression of interferon-γ. Furthermore, in wild-type mice, AngII significantly increased oxidative stress, endothelial cell apoptosis, and endothelial dysfunction. These effects of AngII infusion were significantly suppressed in mice deficient for p47(phox), gp91(phox), or indoleamine-pyrrole 2,3-dioxygenase 1, suggesting that AngII-induced enhancement of Kynurenines via NAD(P)H oxidase-derived oxidants causes endothelial cell apoptosis and dysfunction in vivo. Furthermore, interferon-γ neutralization eliminates AngII-increased superoxide products and endothelial apoptosis by inhibiting AngII-induced Kynurenines generation, suggesting that AngII-activated Kyn pathway is interferon-γ-dependent. Mechanistically, we found that AngII-enhanced 3-hydroxykynurenine promoted the generation of NAD(P)H oxidase-mediated superoxide anions by increasing the translocation and membrane assembly of NAD(P)H oxidase subunits in endothelial cells, resulting in accelerated apoptosis and consequent endothelial dysfunction.Kyn pathway activation accelerates apoptosis and dysfunction of the endothelium by upregulating NAD(P)H-derived superoxide.
Contractually Time-Limited Psychotherapy in an Outpatient Psychosomatic Clinic
Authors: EUGENE MEYER, HERZL R. SPIRO, REGINA SLAUGHTER, IRWIN W. POLLACK, HERBERT WEINGARTNER, SAMUEL NOVEY
Journal: American Journal of Psychiatry (1967)

This report concerns the variables influencing whether a patient showed up for his first psychotherapy appointment, dropped out of therapy, or completed treatment. As single variables, race, sex, age, socioeconomic status, marital status, psychiatric diagnosis, duration of symptoms, and history of parental loss did not relate significantly to completion of therapy. The data thus suggest that, contrary to common belief, patients from the lowest socioeconomic groups can be motivated to complete a program of structured psychotherapy.
Pathological documentation of complete elimination of Barrett's metaplasia following endoscopic multipolar electrocoagulation therapy
Authors: M B Fennerty, C L Corless, B Sheppard, D O Faigel, D A Lieberman, R E Sampliner
Journal: Gut (2001)

The previous paradigm that Barrett9s is an irreversible premalignant lesion has recently been challenged by a proliferation of reports documenting elimination of Barrett9s by a variety of endoscopic techniques. Whether Barrett9s is entirely eliminated is unknown as endoscopic biopsy samples the surface of the epithelium only. Numerous reports document underlying specialised columnar epithelium in many of these trials. Until now there have been no reports of pathological examination of the entire oesophagus as a specimen. This case documents complete elimination of intestinal metaplasia from the oesophagus and supports the biological plausibility of these research techniques.
Leptin Receptor–Related Immune Response in Colorectal Tumors: The Role of Colonocytes and Interleukin-8
Authors: Mohammad Abolhassani, Nijez Aloulou, Marie Thérèse Chaumette, Thomas Aparicio, Nadine Martin-Garcia, Hicham Mansour, Sabine Le Gouvello, Jean Charles Delchier, Iradj Sobhani
Journal: Cancer Research (2008)

Abstract We have shown that ObRb, the leptin receptor, is overexpressed in colorectal cancer cells, and that this may influence the patients' outcome. We investigated colonocytes as leptin targets and characterized their pivotal role in antitumor immune response. Cytokine and chemokine mRNAs in HT29 cells were measured by targeted arrays. In vitro, normal colonocytes and human colon cancer cells (HT29, Caco-2, SW480, and HCT116) were used to investigate ObRb transduction system and cytokine releases. Animal colonocytes and CD8 splenocytes and human HT29, HCT116, and CD8+ cells from blood donors were used to investigate the lymphocyte response to the colonocytes when stimulated by leptin. Leptin-induced cytokine releases in the normal colonic mucosa and tumor growth and cytokine releases within tumors in vivo were measured in male rats and nude mice, respectively. Statistical analysis was done by Fisher's exact and Mann-Whitney U tests. Various cytokines and their receptors were produced in normal and tumoral colonocytes in response to leptin by increasing nuclear factor-κB activation. Interleukin-8 (IL-8) was the main cytokine produced in vitro. The levels of IL-8 and its receptor, CXCR1, were higher in tumors than in homologous normal mucosa. Systemic leptin enhanced the proinflammatory cytokines in normal colonocytes and in HT29 xenografted tumor colonocytes. Colonocyte-derived products after leptin treatment stimulated perforin and granzyme B expressions in normal CD8+ T cells in vitro. Leptin triggers an inflammatory response in tumor tissue by directly stimulating colonocytes, which can recruit T cytotoxic cells in the tumor microenvironment. [Cancer Res 2008;68(22):9423–32]
Republished editorial: Elite athletes' survival advantage
Authors: Adrian E Bauman, Steven N Blair
Journal: British Journal of Sports Medicine (2014)

▸ This article is an abridged version of a paper that was published on bmj.com. Cite this article as: BMJ 2012; 345 :e8338

Two linked papers examine longevity in former Olympic athletes and reach different conclusions.1 2 Clark and colleagues analysed data on 15 174 Olympic medallists from nine countries that have enjoyed success in Olympic Games. The athletes had participated in at least one Olympic Games between 1896 and 2010.1 The study found that Olympic medallists had a relative survival advantage of 8% compared with matched controls, which translates into 2.8 extra years of life. The second and smaller study by Zwiers and colleagues examined data on 9989 people who competed in Olympic Games between 1896 and 1936.2 They reported no increase in survival among those who competed in aerobic sports and higher mortality in those who participated in collision and contact sports, including power sports. Indeed, mixed epidemiological evidence pervades this literature, with many studies identifying a lower risk of mortality in previously elite athletes, especially those competing in aerobic events.3 By contrast, …
Hypersensitivity Pneumonitis Related to Imatinib Mesylate
Authors: A. Bergeron, E. Bergot, G. Vilela, L. Ades, A. Devergie, H. Espérou, G. Socié, F. Calvo, E. Gluckman, P. Ribaud, Ph. Rousselot, A. Tazi
Journal: Journal of Clinical Oncology (2002)

Article Tools SPECIAL DEPARTMENTS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2002.99.179 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 12377975 Hypersensitivity Pneumonitis Related to Imatinib Mesylate A. BergeronxA. BergeronSearch for articles by this author , E. BergotxE. BergotSearch for articles by this author , G. VilelaxG. VilelaSearch for articles by this author , L. AdesxL. AdesSearch for articles by this author , A. DevergiexA. DevergieSearch for articles by this author , H. EspérouxH. EspérouSearch for articles by this author , G. SociéxG. SociéSearch for articles by this author , F. CalvoxF. CalvoSearch for articles by this author , E. GluckmanxE. GluckmanSearch for articles by this author , P. RibaudxP. RibaudSearch for articles by this author , Ph. RousselotxPh. RousselotSearch for articles by this author , A. TazixA. TaziSearch for articles by this author Show More Hôpital de Gonesse, Gonesse, FranceHôpital Saint-Louis, Paris, FranceHôpital Avicenne, Bobigny, France https://doi.org/10.1200/JCO.2002.99.179 First Page Full Text PDF Figures and Tables © 2002 by American Society of Clinical Oncology
Eccrine-centred distribution of human papillomavirus 63 infection in the epidermis of the plantar skin
Authors: K. Egawa
Journal: British Journal of Dermatology (2005)

Summary Background The primary target cell of human papillomaviruses (HPVs) is an unsettled issue. Recent studies have suggested that the hair follicle is an important candidate as the reservoir of certain HPV types. However, little is known about the cells which serve as the target or the reservoir of HPVs in nonhairy palmoplantar skin. Objectives To investigate whether the eccrine sweat gland, the only skin appendage in nonhairy palmoplantar skin, also serves as the target or the reservoir of HPVs. Methods HPV 63‐induced warts were employed in this study, because the virus induces tiny warty lesions of a punctuate appearance in the plantar skin and shows peculiar intracytoplasmic inclusion bodies as a diagnostic histopathological marker of infection: this seemed to provide a useful model for the present study. Serial sections were obtained from the entire body of each biopsy specimen and were investigated histologically, immunohistochemically and using DNA–DNA in situ hybridization (ISH) for the histological localization of HPV 63 infection. Results On microscopy, HPV 63 histopathological changes were seen closely associated with eccrine ducts. Using ISH, HPV 63 DNA was detected not only in keratinocytes resident around acrosyringia but also in the uppermost portion of the eccrine dermal duct. A few keratinocytes harbouring HPV 63 DNA were also identified in acrosyringeal areas in the normal plantar skin adjacent to the wart lesions. Conclusions On the basis of our results, it seems likely that HPV 63 targets keratinocytes resident in or around the eccrine ducts in the plantar skin. The results may also suggest that not only hair follicles but also eccrine ducts serve as reservoirs for certain HPV types, including HPV 63, especially in the nonhairy plantar skin.
Setting up non-commercial clinical trials takes too long in the UK: findings from a prospective study
Authors: Allan Hackshaw, Hannah Farrant, Sue Bulley, Michael J Seckl, Jonathan A Ledermann
Journal: Journal of the Royal Society of Medicine (2008)

Summary Objective To evaluate the specific components of setting up a simple multicentre clinical study four years after the new UK law on clinical trials was implemented in 2004. Design Timelines associated with activating a randomized multicentre trial in lung cancer patients using an investigational medicinal product (statins) were prospectively recorded. Setting 84 trial centres in the UK. Main outcome measures The time taken to go through the three stages necessary to activate a trial at a centre was examined: that is, the time from when Site Specific Information was electronically transferred to a participating centre until local research ethics committee (LREC) or research and development (R&amp;D) approvals were obtained, and a signed Clinical Trials Site Agreement (CTSA) was received. Results It took at least six months to obtain LREC approval in 21% of centres and R&amp;D approval in 52% of centres. Twelve centres (14%) took at least 12 months to obtain R&amp;D approval. 31% of centres took at least three months to return a signed CTSA. Although 52% of centres took at least six months to be activated, 13% were able to complete all three stages in two months or less. Conclusions While some centres can activate trials relatively quickly, there is considerable variation the time taken to set up a trial, much of which is due to the delay in obtaining R&amp;D approval. This is having a major adverse effect on UK health research. There is a national need to streamline the process for considering multi-centre non-commercial clinical trials, in particular, having fixed timelines for R&amp;D assessment. Without this, the costs of trials will increase because of extended duration, and the time to answer a research question and alter clinical practice will be significantly prolonged.