tbuckley/cabot-search huggingface dataset:
Hormonal Markers in Breast Cancer: Coexpression, Relationship with Pathologic Characteristics, and Risk Factor Associations in a Population-Based Study
Authors: Xiaohong R. Yang, Ruth M. Pfeiffer, Montserrat Garcia-Closas, David L. Rimm, Jolanta Lissowska, Louise A. Brinton, Beata Peplonska, Stephen M. Hewitt, Richard W. Cartun, Daniza Mandich, Hironobu Sasano, Dean B. Evans, Thomas R. Sutter, Mark E. Sherman
Journal: Cancer Research (2007)

The objective of this study was to evaluate the coexpression patterns of hormonal markers in breast cancer tissue and their relationship with pathologic characteristics and epidemiologic risk factors. We evaluated the expression of 17 markers by immunohistochemistry in 842 invasive breast carcinomas collected in a population-based case-control study conducted in Poland. Based on marker correlations, factor analysis identified four major coexpression patterns (factors): "nuclear receptor factor" [estrogen receptor (ER)-alpha, progesterone receptor, androgen receptor, cyclin D1, and aromatase], "estrogen metabolism/ER-beta factor" (ER-beta, peroxisome proliferator-activated receptor-gamma, steroid sulfatase, estrogen sulfonotransferase, and cytochrome P450 1B1), "HER2 factor" (human epidermal growth factor receptor 2, E-cadherin, cyclooxygenase-2, aromatase, steroid sulfatase), and "proliferation factor" (cytokeratin 5, cytokeratin 5/6, epidermal growth factor receptor, P53). Three of these factors corresponded to molecular subtypes previously defined by expression profiling; however, the estrogen metabolism/ER-beta factor seemed to be distinctive. High scores for this factor were associated with high tumor grade (P heterogeneity = 0.02), younger age at menarche (P heterogeneity = 0.04), lower current body mass index among premenopausal women (P heterogeneity = 0.01), and older age at menopause (P heterogeneity = 0.04). High scores for the proliferation factor were also associated with early menarche (P heterogeneity < 0.0001), and in contrast to the estrogen metabolism/ER-beta factor, higher current body mass index among premenopausal women (P heterogeneity = 0.03). Our analysis of hormonal pathway markers independently confirmed several previously defined molecular subtypes identified by gene expression profiling and augmented these findings by suggesting the existence of additional relationships related to ER-beta and enzymes involved in hormone metabolism.
Is smoking a risk factor for pneumonia in adults with chickenpox?
Authors: M E Ellis, K R Neal, A K Webb
Journal: BMJ (1987)

<h3>Abstract</h3> <h3>Background</h3> Methods to accurately quantify disease severity are fundamental to plant pathogen interaction studies. Commonly used methods include visual scoring of disease symptoms, tracking pathogen growth <i>in planta</i> over time, and various assays that detect plant defense responses. Several image-based methods for phenotyping of plant disease symptoms have also been developed. Each of these methods has different advantages and limitations which should be carefully considered when choosing an approach and interpreting the results. <h3>Results</h3> In this paper, we developed two image analysis methods and tested their ability to quantify different aspects of disease lesions in the cassava-<i>Xanthomonas</i> pathosystem. The first method uses ImageJ, an open-source platform widely used in the biological sciences. The second method is a few-shot support vector machine learning tool that uses a classifier file trained with five representative infected leaf images for lesion recognition. Cassava leaves were syringe infiltrated with wildtype <i>Xanthomonas</i>, a <i>Xanthomonas</i> mutant with decreased virulence, and mock treatments. Digital images of infected leaves were captured overtime using a Raspberry Pi camera. The image analysis methods were analyzed and compared for the ability to segment the lesion from the background and accurately capture and measure differences between the treatment types. <h3>Conclusions</h3> Both image analysis methods presented in this paper allow for accurate segmentation of disease lesions from the non-infected plant. Specifically, at 4-, 6-, and 9-days post inoculation (DPI), both methods provided quantitative differences in disease symptoms between different treatment types. Thus, either method could be applied to extract information about disease severity. Strengths and weaknesses of each approach are discussed.
Choosing the right path: enhancement of biologically relevant sets of genes or proteins using pathway structure
Authors: Reuben Thomas, Julia M Gohlke, Geffrey F Stopper, Frederick M Parham, Christopher J Portier
Journal: Genome biology (2009)

Abstract A method is proposed that finds enriched pathways relevant to a studied condition using the measured molecular data and also the structural information of the pathway viewed as a network of nodes and edges. Tests are performed using simulated data and genomic data sets and the method is compared to two existing approaches. The analysis provided demonstrates the method proposed is very competitive with the current approaches and also provides biologically relevant results.
Comparison of A1C and Fasting Glucose Criteria to Diagnose Diabetes Among U.S. Adults
Authors: April P. Carson, Kristi Reynolds, Vivian A. Fonseca, Paul Muntner
Journal: Diabetes Care (2009)

To compare A1C and fasting glucose for the diagnosis of diabetes among U.S. adults.This study included 6,890 adults (> or =20 years of age) from the 1999-2006 National Health and Nutrition Examination Survey without a self-reported history of diabetes who had fasted > or =9 h. A1C > or =6.5% and fasting glucose > or =126 mg/dl were used, separately, to define diabetes.Overall, 1.8% of U.S. adults had A1C > or =6.5% and fasting glucose > or =126 mg/dl, 0.5% had A1C > or =6.5% and fasting glucose <126 mg/dl, and 1.8% had A1C <6.5% and fasting glucose > or =126 mg/dl. Compared with individuals with A1C <6.5% and fasting glucose > or =126 mg/dl, individuals with A1C > or =6.5% and fasting glucose <126 mg/dl were younger, more likely to be non-Hispanic black, had lower Hb levels, and had higher C-reactive protein.A1C > or =6.5% demonstrates reasonable agreement with fasting glucose for diagnosing diabetes among U.S. adults.
CD40L-deficient mice show deficits in antiviral immunity and have an impaired memory CD8+ CTL response.
Authors: P Borrow, A Tishon, S Lee, J Xu, I S Grewal, M B Oldstone, R A Flavell
Journal: The Journal of Experimental Medicine (1996)

The ligand for CD40 (CD40L) is expressed on the surface of activated CD4+ T cells and its role in T-B cell collaborations and thymus-dependent humoral immunity is well established. Recently, by generating CD40L-knockout mice, we have confirmed its previously described role in humoral immunity and defined another important function of this molecule in the in vivo clonal expansion of antigen-specific CD4+ T cells. Here, we investigated the potential in vivo role of CD40L in antiviral immunity by examining the immune response mounted by CD40L-deficient mice following infection with lymphocytic choriomeningitis virus (LCMV), Pichinde virus, or vesicular stomatitis virus. Humoral immune responses of CD40L-deficient mice to these viruses were severely compromised, although moderate titres of antiviral IgM and some IgG2a were produced by virus-infected CD40L-deficient mice by a CD4+ T cell-independent mechanism. By contrast, CD40L-deficient mice made strong primary CTL responses to all three viruses. Interestingly however, although memory CTL activity was detectable in CD40L-deficient mice two months after infection with LCMV, the memory CTL response was much less efficient than in wild-type mice. Together, the results show that CD40-CD40L interactions are required for strong antiviral humoral immune responses, and reveal a novel role for CD40L in the establishment and/or maintenance of CD8+ CTL memory.
How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma
Authors: M. Ian Gilmour, Maritta S. Jaakkola, Stephanie J. London, Andre E. Nel, Christine A. Rogers
Journal: Environmental Health Perspectives (2006)

Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur.
Allergic anaphylaxis to Laminaria
Authors: S.R. Knowles, K. Djordjevic, K. Binkley, E.A. Weber
Journal: Allergy (2002)

A patient developed anaphylaxis after insertion of a laminaria tent and laminaria skin testing. Laminaria digitata, a marine kelp, is used in 'tents' for cervical dilation. Laminaria hypersensitivity reactions, including anaphylaxis, are exceedingly rare (1,2). An anaphylactic reaction following insertion of a laminaria tent is described.
A new tool for an old disease
Authors: B. Khanavkar
Journal: European Respiratory Journal (2004)

Over the last two decades, interventional techniques in bronchology, including airway stenting, have become an accepted and widely used method for the relief of critical airway stenoses 1. Currently, main indications are bridgeable malignant stenoses in the course of palliative care. Another field of experience with stents has unfolded in lung transplant surgery with regard to anastomosis problems. In addition, stent placement to consolidate mechanical or laser re-opening of a stenosed bronchus is a feature of “high-tech” medicine 2.

Incidence of tuberculosis in “high-tech” areas has been falling as a result of improved living conditions, as well as effective and timely treatment. Accordingly, bronchial tuberculosis as a late complication in pulmonary tuberculous disease has become a rarity in industrialised countries 3. However, it still remains a considerable clinical problem in high-incidence regions, such as large parts of Africa and Asia 4.

The natural history of bronchial involvement in tuberculosis almost invariably leads to a degree of luminal stricture 5 and, in addition, often remains quite refractory to drug treatment 6. Conversely, early relief of tuberculous bronchial stenosis clearly has the potential to prevent the destruction of pulmonary lobes by atelectasis and bronchiectasis, the so-called post-tuberculous syndrome. In an …
Pathophysiology and fate of hepatocytes in a mouse model of mitochondrial hepatopathies
Authors: F Diaz, S Garcia, D Hernandez, A Regev, A Rebelo, J Oca-Cossio, C T Moraes
Journal: Gut (2007)

Although oxidative phosphorylation defects can affect the liver, these conditions are poorly understood, partially because of the lack of animal models.To create and characterise the pathophysiology of mitochondrial hepatopathies in a mouse model.A mouse model of mitochondrial hepatopathies was created by the conditional liver knockout (KO) of the COX10 gene, which is required for cytochrome c oxidase (COX) function. The onset and progression of biochemical, molecular and clinical phenotypes were analysed in several groups of animals, mostly at postnatal days 23, 56, 78 and 155.Biochemical and histochemical analysis of liver samples from 23-56-day-old KO mice showed liver dysfunction, a severe COX deficiency, marked mitochondrial proliferation and lipid accumulation. Despite these defects, the COX-deficient hepatocytes were not immediately eliminated, and apoptosis followed by liver regeneration could be observed only at age 78 days. Hepatocytes from 56-78-day-old KO mice survived despite very low COX activity but showed a progressive depletion of glycogen stores. In most animals, hepatocytes that escaped COX10 ablation were able to proliferate and completely regenerate the liver between days 78 and 155.The results showed that when faced with a severe oxidative phosphorylation defect, hepatocytes in vivo can rely on glycolysis/glycogenolysis for their bioenergetic needs for relatively long periods. Ultimately, defective hepatocytes undergo apoptosis and are replaced by COX-positive cells first observed in the perivascular regions.
Crohn's disease of the anal region.
Authors: B K Gray, H E Lockhartmummery, B C Morson
Journal: Gut (1965)

EDITORIAL SYNOPSIS This paper records for the first time the clinico-pathological picture of Crohn's disease affecting the anal canal.It has long been recognized that anal lesions may precede intestinal Crohn's disease, often by some years, but the specific characteristics of the lesion have not hitherto been described.The differential diagnosis is discussed in detail.HISTOLOGY Figures 1,4, and 6 all show sarcoid granulomata, as seen in this site.Pieces of tissue for histological examination were taken from all 19 patients at the time of operation for the anal lesion.In every case the anal tissues contained a sarcoid reaction consistent with a diagnosis of Crohn's disease or tuberculosis.The histological sections have been reviewed and in only one case is there any reason to question the original 515 on August 30,
Double-blind randomized pilot trial evaluating the efficacy of oral propranolol on infantile haemangiomas in infants &lt; 4 months of age
Authors: C. Léauté-Labrèze, E. Dumas de la Roque, F. Nacka, A. Abouelfath, N. Grenier, M. Rebola, K. Ezzedine, N. Moore
Journal: British Journal of Dermatology (2013)
Macrophage activation in polyinosinic:polycytidylic acid-accelerated murine lupus nephritis
Authors: Antigoni Triantafyllopoulou, Lionel Ivashkiv
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background and objectives</h3> The inflammatory phase of lupus nephritis is characterised by immune cell infiltrates and develops following the deposition of immune complexes in the kidneys. Immune complex deposition is not sufficient to produce nephritis as first shown by studies of FcRγ<sup>-/-</sup> NZB/W mice (Clynes R <i>et al</i> 1998, Bergtold A <i>et al</i> 2006). The authors have recently identified a population of kidney macrophages, characterised by low surface expression of the myeloid cell marker GR1, which was required for aggressive proliferative lesions and metalloproteinase activity in poly I:C-induced and interferonα- mediated murine lupus nephritis. This population expressed IL-10, IL-1 receptor antagonist, metalloproteinases and growth factors (Triantafyllopoulou A <i>et al</i> PNAS 2010). Here, the authors aimed (A) to identify transcriptional mediators of macrophage activation in lupus nephritis kidneys and (B) to analyse blood monocyte expansion after the onset of proteinuria. <h3>Materials and methods</h3> The authors used the poly I:C model of accelerated lupus nephritis, as previously described. NZB/W mice with spontaneous proteinuria of equal duration, as well as age-matched non-proteinuric mice were used as control groups. Proteinuria was measured by dipstick. Renal disease was assessed by histopathology. Monocyte/macrophage propulations in peripheral blood or single cell suspensions of kidneys were analysed by flow cytometry. Gr1<sup>low</sup> macrophages were analysed by microarrays and real-time PCR (n=2-4 mice per group). <h3>Results</h3> GR1 low monocytes preferentially expand in the peripheral blood of poly I:C - treated nephritic mice as early as after 4 days of proteinuria. Several transcription factors associated with myeloid cell differentiation and inflammatory regulation were identified. Upregulation of IRF-7 was of particular interest and was confirmed by real time PCR. <h3>Conclusions</h3> The expansion of GR1<sup>low</sup> monocytes in a macrophage-driven model of crescentic lupus nephritis occurs at an early stage of disease in the peripheral blood compartment, thus suggesting that monocytes may be activated in lupus nephritis before their entry in the kidneys. Upregulated IRF-7 expression in infiltrating kidney macrophages suggests that macrophage-derived type I interferons may be crucial for proliferative lesions and accelerated glomerular damage.
Coeliac disease and malignancy of the duodenum: diagnosis by endoscopy, successful treatment of the malignancy, and response to a gluten free diet.
Authors: M J Hall, B T Cooper, N Rooney, H Thompson, A E Read
Journal: Gut (1991)

A patient presented with subtotal villous atrophy and a malignant duodenal tumour of uncertain histogenesis. He was successfully treated by resection and chemotherapy and the small bowel mucosa recovered on a gluten free diet. The tumour was diagnosed at upper gastrointestinal endoscopy when barium studies and abdominal computed tomography were normal, thus making this one of the earliest coeliac malignancies diagnosed.
Organisation of safety measures in an Alpine World Junior Championship
Authors: K A Bergstrøm, A Bergstrøm, A Ekeland
Journal: British Journal of Sports Medicine (2001)

To study the implementation of skiing safety during the Alpine World Junior Championship of 1995.A map of the area was made with descriptions of the slopes and all its facilities and the security measures along the course. The number of competitors who started and any injuries reported were recorded in a questionnaire.A total of 452 girls and 546 boys started in the different races. Only four injuries were recorded, all in girls. The overall injury rate was 4 per 1000 runs. An injury rate of 8.3 per 1000 runs was recorded in the downhill. One skier had a possibly severe injury (ISS = 14) in the downhill; the rest of the injuries were minor (ISS = 1). The mean ISS was 4.3 and the total ISS was 17.A significantly higher injury rate was recorded for young female than young male racers. The injury rate was significantly higher in downhill than the other alpine disciplines in the Alpine World Junior Championship. The injury rate was not significantly different from that recorded one year previously for Olympic racers, and juniors therefore need the same safety measures as Olympic racers.
Response to Letter Regarding Article, “Early Treatment With Lisinopril and Spironolactone Preserves Cardiac and Skeletal Muscle in Duchenne Muscular Dystrophy Mice”
Authors: Jill A. Rafael-Fortney, Neeraj S. Chimanji, Kevin E. Schill, Christopher D. Martin, Jason D. Murray, Jenna E. Stangland, Ying Xu, Benjamin D. Canan, Ranjit Ganguly, Tessily A. Mays, Dawn A. Delfín, Tam Tran, Paul M.L. Janssen, Subha V. Raman
Journal: Circulation (2012)
Prospective Study of Long-Term Impact of Adjuvant High-Dose and Conventional-Dose Chemotherapy on Health-Related Quality of Life
Authors: Ciska Buijs, Sjoerd Rodenhuis, Caroline M. Seynaeve, Quirinus G.C.M. van Hoesel, Elsken van der Wall, Wim J.M. Smit, Marianne A. Nooij, Emile Voest, Pierre Hupperets, Els M. TenVergert, Harm van Tinteren, Pax H.B. Willemse, Marian J.E. Mourits, Neil K. Aaronson, Wendy J. Post, Elisabeth G.E. de Vries
Journal: Journal of Clinical Oncology (2007)

To evaluate and compare health-related quality of life (HRQOL) after conventional- and high-dose adjuvant chemotherapy in patients with high-risk breast cancer.Patients were randomly assigned to either a conventional or high-dose chemotherapy regimen; both regimens were followed by radiotherapy and tamoxifen. HRQOL was evaluated until disease progression using the Short Form-36 (SF-36), Visual Analog Scale, and Rotterdam Symptom Checklist and assessed every 6 months for 5 years after random assignment. For the SF-36, data from healthy Dutch women with the same age distribution served as reference values.Eight hundred four patients (conventional-dose chemotherapy, n = 405; high-dose chemotherapy, n = 399) were included. Median follow-up time was 57 months. Directly after high-dose chemotherapy, HRQOL decreased more compared with conventional chemotherapy for all SF-36 subscales. After 1 year, the reference value of healthy women was reached in both groups. Small differences were observed between the two groups in the role-physical and role-emotional subscales, but 1 year after treatment, these differences were minor and not clinically relevant. During follow-up, patients with a lower educational level and many complaints before chemotherapy experienced a worse HRQOL.Shortly after high-dose chemotherapy, HRQOL was more affected than after conventional-dose chemotherapy. One year after random assignment, differences were negligible. Identifying patients who have a higher chance of persistent impaired quality of life after treatment (which, in the present study, included patients with a lower educational level and many complaints before chemotherapy) is important and may open the way for better patient-tailored prevention strategies.
Tumor cell entry into the lymph node is controlled by CCL1 chemokine expressed by lymph node lymphatic sinuses
Authors: Suvendu Das, Eliana Sarrou, Simona Podgrabinska, Melanie Cassella, Sathish Kumar Mungamuri, Nikki Feirt, Ronald Gordon, Chandandeep S. Nagi, Yarong Wang, David Entenberg, John Condeelis, Mihaela Skobe
Journal: The Journal of Experimental Medicine (2013)

Lymphatic vessels are thought to contribute to metastasis primarily by serving as a transportation system. It is widely believed that tumor cells enter lymph nodes passively by the flow of lymph. We demonstrate that lymph node lymphatic sinuses control tumor cell entry into the lymph node, which requires active tumor cell migration. In human and mouse tissues, CCL1 protein is detected in lymph node lymphatic sinuses but not in the peripheral lymphatics. CCR8, the receptor for CCL1, is strongly expressed by human malignant melanoma. Tumor cell migration to lymphatic endothelial cells (LECs) in vitro is inhibited by blocking CCR8 or CCL1, and recombinant CCL1 promotes migration of CCR8+ tumor cells. The proinflammatory mediators TNF, IL-1β, and LPS increase CCL1 production by LECs and tumor cell migration to LECs. In a mouse model, blocking CCR8 with the soluble antagonist or knockdown with shRNA significantly decreased lymph node metastasis. Notably, inhibition of CCR8 led to the arrest of tumor cells in the collecting lymphatic vessels at the junction with the lymph node subcapsular sinus. These data identify a novel function for CCL1–CCR8 in metastasis and lymph node LECs as a critical checkpoint for the entry of metastases into the lymph nodes.