tbuckley/cabot-search huggingface dataset:
Cow's Milk and Linear Growth in Industrialized and Developing Countries
Authors: Camilla Hoppe, Christian Mølgaard, Kim F. Michaelsen
Journal: Annual Review of Nutrition (2006)

▪ Abstract The strongest evidence that cow's milk stimulates linear growth comes from observational and intervention studies in developing countries that show considerable effects. Additionally, many observational studies from well-nourished populations also show an association between milk intake and growth. These results suggest that milk has a growth-stimulating effect even in situations where the nutrient intake is adequate. This effect is supported by studies that show milk intake stimulates circulating insulin-like growth factor (IGF)-I, which suggests that at least part of the growth-stimulating effects of milk occur through the stimulation of IGFs. Given that the biological purpose of milk is to support the newborn during a period of high growth velocity, such an effect seems plausible. Adding cow's milk to the diet of stunted children is likely to improve linear growth and thereby reduce morbidity. In well-nourished children, the long-term consequences of an increased consumption of cow's milk, which may lead to higher levels of IGF-I in circulation or an increase in the velocity of linear growth, are likely to be both positive and negative. Based on emerging data that suggest both growth and diet during early life program the IGF axis, the association between milk intake and later health is likely to be complex. [ Notice ]
Changes in anteroposterior patellar tendon diameter support a continuum of pathological changes
Authors: Peter Malliaras, Jill Cook
Journal: British Journal of Sports Medicine (2011)

A continuum of pathological ultrasound patellar tendon changes from normal tendons, followed by diffuse and then focal change in echogenicity has been proposed. The anteroposterior (AP) diameter of each pathological state and whether change in pathological state is accompanied by change in AP diameter are not known. The aims of this study were to (1) investigate the AP diameter of previously described patellar tendon ultrasound groups (normal, diffuse and focal change in echogenicity) and (2) investigate the change in AP diameter among active volleyball players during a season and whether this corresponds with change in ultrasound group.The grey-scale ultrasound pathological groups (normal, diffuse, focal) and AP diameter were measured among 102 volleyball players at the beginning of a season and 58 volleyball players at 6 one-monthly intervals during a 5-month indoor season.There was a significant ordinal relationship (analysis of variance, Student-Neuman-Keuls post hoc test, p < 0.05) between AP diameter and normal tendons, diffuse and focally abnormal tendons among men (3.4 ± 0.4, 4.9 ± 0.4, 6.5 ± 1.8 mm) and women (3.2 ± 0.4, 4.2 ± 0.4, 4.6 ± 0.7 mm). Tendons that stayed in the same group tended to have a smaller mean change than tendons that changed group.These findings support the proposed continuum of tendon pathology. Mild patellar tendon thickening (>4.2 mm among men, >4 mm among women) may indicate pathology among active athletes.
Impact of tumor HPV status on outcome in patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck receiving chemotherapy with or without cetuximab: retrospective analysis of the phase III EXTREME trial
Authors: J.B. Vermorken, A. Psyrri, R. Mesía, F. Peyrade, F. Beier, B. de Blas, I. Celik, L. Licitra
Journal: Annals of Oncology (2014)

BackgroundTumor human papillomavirus (HPV) status is an important prognostic factor in locoregionally advanced squamous cell carcinoma of the head and neck (SCCHN). Prognostic value in recurrent and/or metastatic (R/M) disease remains to be confirmed. This retrospective analysis of the EXTREME trial, comparing chemotherapy plus cetuximab with chemotherapy first line in R/M SCCHN, investigated efficacy and prognosis according to tumor p16 and HPV status.Patients and methodsPaired tissue samples were used: p16INK4A expression was assessed by immunohistochemistry, and HPV status determined in extracted DNA samples using oligonucleotide hybridization assays.ResultsAltogether, 416 of 442 patients had tumor samples available for p16 and HPV: 10% of tumors were p16 positive and 5% were HPV positive. Adding cetuximab to chemotherapy improved survival, irrespective of tumor p16 or HPV status. This pattern remained in a combined analysis of p16 and HPV. p16 positivity and HPV positivity were associated with prolonged survival compared with p16 negativity and HPV negativity. Subgroup analysis of patients with oropharyngeal cancer demonstrated a similar pattern to all evaluable patients.ConclusionThe results from this analysis suggest that p16 and HPV status have prognostic value in R/M SCCHN and survival benefits of chemotherapy plus cetuximab over chemotherapy alone are independent of tumor p16 and HPV status.
Coexistence of Differentiated Thyroid Carcinoma With Primary Thyroid Lymphoma in a Background of Hashimoto's Thyroiditis
Authors: Evangeline Vassilatou, Theofanis Economopoulos, Marinella Tzanela, Dimitra Rontogianni, Petros Karakitsos, Christina Magou, Dimitrios Hadjidakis, George Dimitriadis
Journal: Journal of Clinical Oncology (2011)
Alpha-4 integrins and VCAM-1, but not MAdCAM-1, are essential for recruitment of mast cell progenitors to the inflamed lung
Authors: J. Pablo Abonia, Jenny Hallgren, Tatiana Jones, Tong Shi, Yuhui Xu, Pandelakis Koni, Richard A. Flavell, Joshua A. Boyce, K. Frank Austen, Michael F. Gurish
Journal: Blood (2006)
Influence of obesity on the risk of developing colon cancer
Authors: E E Frezza
Journal: Gut (2005)

Obesity is a risk factor for many diseases.Thirty per cent of Americans are viewed as super obese; therefore, we need to find a solution.We already know about the diseases associated with obesity such as high blood pressure, diabetes, sleep apnoea, etc. Lately, there has been an increased interest in understanding if cancer is related to obesity.In this paper, we review the incidence of colon cancer and obesity.Insulin is the best established biochemical mediator between obesity and colon cancer.Hyperinsulinaemia, such as occurs in type II diabetes, is important in the pathogenesis of colon cancer.All adipose tissue is not equal.Visceral abdominal fat has been identified as the essential fat depot for pathogenetic theories that relate obesity and colon cancer.The genders differ as regards to how the relationship between obesity and colon cancer has been evaluated.Obesity imposes a greater risk of colon cancer for men of all ages and for premenopausal women than it does for postmenopausal women.Regular exercise reduces the risk of developing colon cancer and the risk of death from colon cancer should it develop.We believe that a combination of waist circumference (WC) and body mass index (BMI) measurements is recommended to assess the obesity related risk of developing colon cancer.Radiographic assessments of visceral abdominal fat may eventually prove to be the best means of assessing a patient's obesity related risk of developing colon cancer.Although WC is better established as a measure of obesity than BMI, the evidence for colon cancer risk is not secure on this point; combining BMI and WC measurements would appear, at present, to be the wisest approach for colon cancer risk assessment.Doctors who wish to decrease their patients' risk of dying of colon cancer should advise weight loss and exercise.Conversely, physicians and public health authorities should consider both exercise and obesity when designing colon cancer screening protocols.Morphometric cut offs should be adjusted, if possible, for age, sex, ethnicity, and height.
Predictive and prognostic factors for treatment and survival in 305 patients with advanced gastrointestinal neuroendocrine carcinoma (WHO G3): The NORDIC NEC study
Authors: H. Sorbye, S. Welin, S.W. Langer, L.W. Vestermark, N. Holt, P. Osterlund, S. Dueland, E. Hofsli, M.G. Guren, K. Ohrling, E. Birkemeyer, E. Thiis-Evensen, M. Biagini, H. Gronbaek, L.M. Soveri, I.H. Olsen, B. Federspiel, J. Assmus, E.T. Janson, U. Knigge
Journal: Annals of Oncology (2012)
Mutations in the Genes for Cardiac Troponin T and α-Tropomyosin in Hypertrophic Cardiomyopathy
Authors: Hugh Watkins, William J. McKenna, Ludwig Thierfelder, H. Jacqueline Suk, Ryuichiro Anan, Annie O'Donoghue, Paolo Spirito, Akira Matsumori, Christine S. Moravec, J.G. Seidman, Christine E. Seidman
Journal: New England Journal of Medicine (1995)

Familial hypertrophic cardiomyopathy can be caused by mutations in the genes for beta cardiac myosin heavy chain, alpha-tropomyosin, or cardiac troponin T. It is not known how often the disease is caused by mutations in the tropomyosin and troponin genes, and the associated clinical phenotypes have not been carefully studied.Linkage between polymorphisms of the alpha-tropomyosin gene or the cardiac troponin T gene and hypertrophic cardiomyopathy was assessed in 27 families. In addition, 100 probands were screened for mutations in the alpha-tropomyosin gene, and 26 were screened for mutations in the cardiac troponin T gene. Life expectancy, the incidence of sudden death, and the extent of left ventricular hypertrophy were compared in patients with different mutations.Genetic analyses identified only one alpha-tropomyosin mutation, identical to one previously described. Five novel mutations in cardiac troponin were identified, as well as a further example of a previously described mutation. The clinical phenotype of four troponin T mutations in seven unrelated families was similar and was characterized by a poor prognosis (life expectancy, approximately 35 years) and a high incidence of sudden death. The mean (+/- SD) maximal thickness of the left ventricular wall in subjects with cardiac troponin T mutations (16.7 +/- 5.5 mm) was significantly less than that in subjects with beta cardiac myosin heavy-chain mutations (23.7 +/- 7.7 mm, P < 0.001).Mutations in alpha-tropomyosin are a rare cause of familial hypertrophic cardiomyopathy, accounting for approximately 3 percent of cases. Mutations in cardiac troponin T account for approximately 15 percent of cases of familial hypertrophic cardiomyopathy in this referral-center population. These mutations are characterized by relatively mild and sometimes subclinical hypertrophy but a high incidence of sudden death. Genetic testing may therefore be especially important in this group.
Treatment of Hemorrhoids
Authors: A. W. Martin Marino
Journal: JAMA (1969)

<h3>To the Editor:—</h3> In our comment (<b>205</b>:469, 1968) we attempted to make the following three points: (1) the responsibility to employ all available diagnostic modalities to rule out a cause of bleeding proximal to internal hemorrhoids; (2) that hemorrhoidectomy can be performed in such a way that it is not "extremely unpleasant"; and (3) that ligation of internal hemorrhoids is an adjunct rather than a panacea. Blaisdell (<b>206</b>:1793, 1968) commented on our "few months" experience and his "18 years" thereof. It is true that we have used office ligation techniques for only 4 1/2 years. We believe the time sufficient to enable an objective evaluation of a procedure. Blaisdell maintains that our evaluation of the symptoms of anorectal disease and pathology (based on anatomic principles and acknowledged concepts of anorectal innervation) is "just not so." As justification for this he offers his clinical evaluation of the results obtained
A Novel MAPK–microRNA Signature Is Predictive of Hormone-Therapy Resistance and Poor Outcome in ER-Positive Breast Cancer
Authors: Philip C. Miller, Jennifer Clarke, Tulay Koru-Sengul, Joeli Brinkman, Dorraya El-Ashry
Journal: Clinical Cancer Research (2014)

Abstract Purpose: Hyperactivation of ERK1/2 MAPK (hMAPK) leads to loss of estrogen receptor (ER) expression and poor outcome in breast cancer. microRNAs (miRNA) play important regulatory roles and serve as biomarkers of disease. Here, we describe molecular, pathologic, and clinical outcome associations of an hMAPK–miRNA expression signature in breast cancer. Experimental Design: An hMAPK–miRNA signature was identified, and associations of this signature with molecular and genetic alterations, gene expression, pathologic features, and clinical outcomes were determined in primary breast cancers from training data and validated using independent datasets. Univariate and multivariate analyses identified subsignatures associated with increased disease recurrence and poorer disease survival among ER-positive (ER+) patients, respectively. Results: High-hMAPK–miRNA status significantly correlated with ER-negativity, enrichment for basal and HER2-subtypes, and reduced recurrence-free and disease-specific survival in publicly available datasets. A robust determination of a recurrence signature and a survival signature identified hMAPK–miRNAs commonly associated with poor clinical outcome, and specific subsets associated more closely with either disease recurrence or disease survival, especially among ER+ cancers of both luminal A and luminal B subtypes. Multivariate analyses indicated that these recurrence and survival signatures significantly associated with increased risk of disease-specific death and disease recurrence in ER+ cancer and ER+ cancers treated with hormone therapy. Conclusions: We report an hMAPK–miRNA signature and two subsignatures derived from it that associate significantly with adverse clinical features, poor clinical outcome, and poor response to hormone therapy in breast cancer, thus identifying potential effectors of MAPK signaling, and novel predictive and prognostic biomarkers or therapeutic targets in breast cancer. Clin Cancer Res; 21(2); 373–85. ©2014 AACR.
IL-9 Governs Allergen-induced Mast Cell Numbers in the Lung and Chronic Remodeling of the Airways
Authors: Jennifer Kearley, Jonas S Erjefalt, Cecilia Andersson, Ebony Benjamin, Carla P Jones, Annette Robichaud, Sophie Pegorier, Yambasu Brewah, Timothy J Burwell, Leif Bjermer, Peter A Kiener, Roland Kolbeck, Clare M Lloyd, Anthony J Coyle, Alison A Humbles
Journal: American Journal of Respiratory and Critical Care Medicine (2010)

IL-9 is a pleiotropic cytokine that has multiple effects on structural as well as numerous hematopoietic cells, which are central to the pathogenesis of asthma.
Role of Human Cripto-1 in Tumor Angiogenesis
Authors: Caterina Bianco, Luigi Strizzi, Andreas Ebert, Cindy Chang, Aasia Rehman, Nicola Normanno, Liliana Guedez, Rita Salloum, Erika Ginsburg, Youping Sun, Nadia Khan, Morihisa Hirota, Brenda Wallace-Jones, Christian Wechselberger, Barbara K Vonderhaar, Giovanna Tosato, William G Stetler-Stevenson, Michele Sanicola, David S Salomon
Journal: JNCI Journal of the National Cancer Institute (2005)

Background: Human cripto-1 (CR-1) promotes cell transformation and increases migration and invasion of various mouse and human epithelial cell lines. We investigated whether CR-1 also stimulates angiogenesis. Methods: We used human umbilical vein endothelial cells (HUVECs) to measure in vitro migration with fibronectin-coated Boyden chambers, invasion with Matrigel-coated Boyden chambers, proliferation with a tetrazolium salt, and differentiation with an in vitro Matrigel assay. We investigated new blood vessel formation in vivo by use of Matrigel-filled silicone cylinders implanted under the skin of nude mice and by use of a breast cancer xenograft model with CR-1-transfected or control Neo-transfected MCF-7 human breast cancer cells. We also used a blocking anti-CR-1 monoclonal antibody to investigate the role of CR-1 in angiogenesis in vivo and in vitro. All statistical tests were two-sided. Results: CR-1 stimulated HUVEC proliferation, migration, and invasion and induced HUVEC differentiation into vascular-like structures on Matrigel. In vivo, recombinant CR-1 protein induced microvessel formation in Matrigel-filled silicone cylinders, and microvessel formation was statistically significantly inhibited with a blocking anti-CR-1 monoclonal antibody (CR-1 and antibody = 127% of microvessel formation compared with that in untreated control cylinders and CR-1 alone = 259%; difference = 132%, 95% confidence interval [CI] = 123% to 140%; P <.001). Tumors formed by CR-1-transfected MCF-7 cells in the cleared mammary fat pad of nude mice had higher microvessel density than tumors formed by control Neo-transfected MCF-7 cells (CR-1-transfected cells = 4.66 vessels per field and Neo-transfected cells = 2.33 vessels per field; difference = 2.33 vessels per field, 95% CI = 1.2 to 2.8; P = .004). Conclusion: CR-1 appears to have an important role in the multistep process of angiogenesis.
Safe at School: A Virginia Experience
Authors: Martha A. Hellems, William L. Clarke
Journal: Diabetes Care (2007)

The Commonwealth of Virginia passed legislation in 1999 requiring nonmedical school personnel to assist students with the management of type 1 diabetes when school nurses were unavailable. This study was designed to determine which school personnel in Virginia currently assist type 1 diabetic students with insulin administration and management of hypoglycemia and to determine if these students are being cared for in a safe manner.Parents of children with type 1 diabetes who attended public school in Virginia during the previous year and who were receiving their diabetes care at the University of Virginia diabetes clinics were asked to participate in an anonymous survey. The survey asked parents which school personnel were responsible for their child's diabetes care while at school and which persons helped with specific care tasks including blood glucose monitoring, insulin administration, and assistance with treatment of hypoglycemia. Questions were asked regarding the occurrence and treatment of hypoglycemia and any adverse effects of such treatment.A total of 185 parents whose children attended 153 different schools responded, 69% of whom reported that a full-time school nurse was assigned to their child's school. In other schools, teachers, administrators, coaches, and cafeteria workers supplemented part-time nurses in assisting students with diabetes management tasks. Although hypoglycemia was not a rare event (75% of students experienced a median of five episodes per year), only one severe event requiring the use of glucagon was reported. In that case, glucagon was administered appropriately by a part-time school nurse, and the student experienced no adverse effects related to the treatment.Students with type 1 diabetes can be cared for safely during the school day by a variety of trained medical and nonmedical personnel. The occurrence of one severe hypoglycemic event among 185 students suggests that as many as 3% of students could experience severe hypoglycemia in a given school year. Legislation that permits nonmedical school personnel to assist students with their diabetes management could make the diabetic children's school day safer and improve their overall glucose control.
Intensive Therapy With Growth Factor Support for Patients With Ewing Tumor Metastatic at Diagnosis: Pediatric Oncology Group/Children's Cancer Group Phase II Study 9457—A Report From the Children's Oncology Group
Authors: Mark L. Bernstein, Meenakshi Devidas, Dominique Lafreniere, Abdul-Kader Souid, Paul A. Meyers, Mark Gebhardt, Kimo Stine, Richard Nicholas, Elizabeth J. Perlman, Ronald Dubowy, Irving W. Wainer, Paul S. Dickman, Michael P. Link, Allen Goorin, Holcombe E. Grier
Journal: Journal of Clinical Oncology (2005)

Prognosis is poor for Ewing sarcoma patients with metastasis at diagnosis. We intensified a five-drug therapy (ifosfamide, etoposide alternated with vincristine, doxorubicin, and cyclophosphamide) using filgrastim but not stem-cell support. We studied topotecan alone and combined with cyclophosphamide in therapeutic windows before the five-drug therapy. A randomly assigned proportion of patients received amifostine as a cytoprotective agent.Eligible patients were < or = 30 years old and had histologically proven Ewing sarcoma or primitive neuroectodermal tumor (PNET) and metastasis at diagnosis. Chemotherapeutic cycles began every 21 days, after recovery from toxicities.One hundred ten of the 117 patients enrolled were eligible. Thirty-six patients received initial topotecan. Three had partial responses (PRs), and 17 had progressive disease (PD). Thirty-seven patients were administered topotecan and cyclophosphamide; 21 of these patients achieved PR, and one patient had PD. In a randomly assigned group of 69 patients, amifostine did not provide myeloprotection, which was measured by absolute neutrophil count, platelet count, or cycle intervals. The best responses to the overall therapy included 45 complete responses, 41 PRs, stable disease in 14 patients, and PD in five patients. For all patients, the 2-year event-free survival (EFS) rate was 24% (+/- 4%), and the overall survival rate was 46% (+/- 5%). For the 39 patients with isolated pulmonary metastases, the 2-year EFS rate was 31% (+/- 7%) compared with 20% (+/- 5%) for patients with more widespread disease.Topotecan had limited activity in patients with Ewing sarcoma or PNET metastatic at diagnosis. The topotecan-cyclophosphamide combination was active. Amifostine was not myeloprotective. Overall results showed no improvement compared with previous studies.
A metalloprotease inhibitor blocks shedding of the 80-kD TNF receptor and TNF processing in T lymphocytes.
Authors: P D Crowe, B N Walter, K M Mohler, C Otten-Evans, R A Black, C F Ware
Journal: The Journal of Experimental Medicine (1995)

TNF is synthesized as a 26-kD membrane-anchored precursor and is proteolytically processed at the cell surface to yield the mature secreted 17-kD polypeptide. The 80-kD tumor necrosis factor (TNF) receptor (TNFR80) is also proteolytically cleaved at the cell surface (shed), releasing a soluble ligand-binding receptor fragment. Since processing of TNF and TNFR80 occurs concurrently in activated T cells, we asked whether a common protease may be involved. Here, we present evidence that a recently described inhibitor of TNF processing N-(D,L-[2-(hydroxyaminocarbonyl)methyl]-4-methylpentanoyl)L- 3-(2'naphthyl)- alanyl-L-alanine, 2-aminoethyl amide (TAPI) also blocks shedding of TNFR80, suggesting that these processes may be coordinately regulated during T cell activation. In addition, studies of murine fibroblasts transfected with human TNFR80, or a cytoplasmic deletion form of TNFR80, reveal that inhibition of TNFR80 shedding by TAPI is independent of receptor phosphorylation and does not require the receptor cytoplasmic domain.
Stem Cell Bioengineering
Authors: Peter W. Zandstra, Andras Nagy
Journal: Annual Review of Biomedical Engineering (2001)

▪ Abstract Tissue engineering and cellular therapies, either on their own or in combination with therapeutic gene delivery, have the potential to significantly impact medicine. Implementation of technologies based on these approaches requires a readily available source of cells for the generation of cells and tissues outside a living body. Because of their unique capacity to regenerate functional tissue for the lifetime of an organism, stem cells are an attractive “raw material” for multiple biotechnological applications. By definition they are self-renewing because on cell division they can generate daughter stem cells. They are also multipotent because they can differentiate into numerous specialized, functional cells. Recent findings have shown that stem cells exist in most, if not all, tissues, and that stem cell tissue specificity may be more flexible than originally thought. Although the potential for producing novel cell-based products from stem cells is large, currently there are no effective technologically relevant methodologies for culturing stem cells outside the body, or for reproducibly stimulating them to differentiate into functional cells. A mechanistic understanding of the parameters important in the control of stem cell self-renewal and lineage commitment is thus necessary to guide the development of bioprocesses for the ex vivo culture of stem cells and their derivates.