tbuckley/cabot-search huggingface dataset:
Prevalence and Distribution of Murine Mammary Tumor Virus Antigen Detectable by Immunocytochemistry in Spontaneous Breast Tumors of Wild Mice&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: M B Gardner, J K Lund, R D Cardiff
Journal: JNCI Journal of the National Cancer Institute (1980)

Mouse mammary tumor virus (MuMTV) antigens were detected by immunoperoxidase cytochemistry in spontaneous breast tumors of wild mice from two widely separated areas of southern California. Eleven of 25 (44%) tumors from Lake Casitas (LC) mice and 4 of 5 tumors from Bouquet Canyon mice were positive. Included among the tumors lacking detectable MuMTV antigen were well-differentiated type A and type B carcinomas as well as tumors with an atypical pattern. In the antigen-positive tumors the distribution of staining was patchy and extremely variable in extent (less than 1-70% stained cells). The intensity and extent of staining were generally greater in breast tumors from hybrids of LC wild mice and C5LBL/10Sn or AKR inbred mice. A good correlation was found in the same tumors between immunoperoxidase staining, detection of MuMTV gp52 antigen by radioimmunoassay, and detection of type B particles by electron microscopy. All of the breast tumors in LC mice were positive for type C virus particles.
Risk for metabolic control problems in minority youth with diabetes.
Authors: A M Delamater, K H Shaw, E B Applegate, I A Pratt, M Eidson, G X Lancelotta, L Gonzalez-Mendoza, S Richton
Journal: Diabetes Care (1999)

OBJECTIVE: We examined and quantified the degree of risk for poor glycemic control and hospitalizations for diabetic ketoacidosis (DKA) among black, Hispanic, and white children and adolescents with diabetes. RESEARCH DESIGN AND METHODS: We examined ethnic differences in metabolic control among 68 black, 145 Hispanic, and 44 white children and adolescents with type 1 diabetes (mean age 12.9 [range 1-21] years), who were primarily of low socioeconomic status. Clinical and demographic data were obtained by medical chart review. Glycohemoglobins were standardized and compared across ethnic groups. Odds ratios among the ethnic groups for poor glycemic control and hospitalizations for DKA were also calculated. RESULTS: The ethnic groups were not different with respect to age, BMI, insulin dose, or hospitalizations for DKA, but black children were older at the time of diagnosis than Hispanics (P &amp;lt; 0.05) and were less likely to have private health insurance than white and Hispanic children (P &amp;lt; 0.001). Black youths had higher glycohemoglobin levels than white and Hispanic youths (P &amp;lt; 0.001 after controlling for age at diagnosis). Black youths were also at greatest risk for poor glycemic control (OR = 3.9, relative to whites; OR = 2.5, relative to Hispanics). CONCLUSIONS: These results underscore and quantify the increased risk for glycemic control problems of lower-income, black children with diabetes. In the absence of effective intervention, these youths are likely to be overrepresented in the health care system as a result of increased health complications related to diabetes.
The Human T Cell Receptor in Health and Disease
Authors: Paul A. H. Moss, William M. C. Rosenberg, John I. Bell
Journal: Annual Review of Immunology (1992)

The T cell antigen receptor (TCR) recognizes antigen in the form short peptides bound to a major histocompatibility (MHC) molecule. This review provides a synopsis of the current state of knowledge of the structure and function of the receptor and its possible role in human disease. Analysis of the T cell receptor usage of T-cell lines and clones recognizing the same peptide-MHC complex is beginning to shed light onto the structural basis of the TCR-peptide-MHC complex. Also, it is now apparent that there are two mechanisms by which the TCR can interact with the MHC molecule, either through classical peptide interactions or through superantigens. Finally, we review the role of specific TCRs in human disease. Current evidence in this area is difficult to interpret; however, it is likely that TCR-mediatedi sease susceptibility exists, and its basis at either a germline or somatic level will soon be clarified.
Long-term persistence of donor nuclei in a Duchenne muscular dystrophy patient receiving bone marrow transplantation
Authors: Emanuela Gussoni, Richard R. Bennett, Kristina R. Muskiewicz, Todd Meyerrose, Jan A. Nolta, Irene Gilgoff, James Stein, Yiu-mo Chan, Hart G. Lidov, Carsten G. Bönnemann, Arpad von Moers, Glenn E. Morris, Johan T. den Dunnen, Jeffrey S. Chamberlain, Louis M. Kunkel, Kenneth Weinberg
Journal: Journal of Clinical Investigation (2002)

Duchenne muscular dystrophy (DMD) is a severe progressive muscle-wasting disorder caused by mutations in the dystrophin gene. Studies have shown that bone marrow cells transplanted into lethally irradiated mdx mice, the mouse model of DMD, can become part of skeletal muscle myofibers. Whether human marrow cells also have this ability is unknown. Here we report the analysis of muscle biopsies from a DMD patient (DMD-BMT1) who received bone marrow transplantation at age 1 year for X-linked severe combined immune deficiency and who was diagnosed with DMD at age 12 years. Analysis of muscle biopsies from DMD-BMT1 revealed the presence of donor nuclei within a small number of muscle myofibers (0.5-0.9%). The majority of the myofibers produce a truncated, in-frame isoform of dystrophin lacking exons 44 and 45 (not wild-type). The presence of bone marrow-derived donor nuclei in the muscle of this patient documents the ability of exogenous human bone marrow cells to fuse into skeletal muscle and persist up to 13 years after transplantation.
Effects of phosphorylation of troponin I and C protein on isometric tension and velocity of unloaded shortening in skinned single cardiac myocytes from rats.
Authors: P A Hofmann, J H Lange
Journal: Circulation Research (1994)

Effects on isometric tension generation and maximum velocity of unloaded shortening after exposure to cAMP-dependent protein kinase (PKA) were investigated in rat enzymatically isolated, tritonized ventricular myocytes. Exposure of myocytes to PKA in the presence of [32P]ATP resulted in phosphorylation of troponin I and C protein. Ca2+ sensitivity of isometric tension was assessed as pCa50, ie, the [Ca2+] at which tension was 50% of maximum, and was lower after PKA treatment (pCa50 5.58) than before PKA treatment (pCa50 5.74). This suggests beta-adrenergic stimulation of the heart and subsequent increases in PKA activity and phosphorylation of troponin I and C protein lead to a significant decrease in tension-generating ability at a given submaximum [Ca2+]. Unloaded shortening velocity was determined by measuring the time required to take up various amounts of slack imposed at one end of the cardiac myocyte preparation. Unloaded shortening velocity during maximum activation was 2.88 +/- 0.11 muscle lengths per second (mean +/- SEM) before PKA exposure and 2.86 +/- 0.13 muscle lengths per second after PKA exposure. Unloaded shortening velocity during 40% of maximum activation was 1.91 +/- 0.25 muscle lengths per second before PKA exposure and 2.17 +/- 0.15 muscle lengths per second after PKA exposure. The absence of an effect of PKA on unloaded shortening velocity in skinned ventricular myocytes suggests that beta-adrenergic stimulation of myocardium either does not affect myofilament velocity of shortening or alters velocity of shortening by a non-PKA-dependent process.
The influence of letrozole on serum lipid concentrations in postmenopausal women with primary breast cancer who have completed 5 years of adjuvant tamoxifen (NCIC CTG MA.17L)
Authors: K.M. Wasan, P.E. Goss, P.H. Pritchard, L. Shepherd, M.J. Palmer, S. Liu, D. Tu, J.N. Ingle, M. Heath, D. DeAngelis, E.A. Perez
Journal: Annals of Oncology (2005)
Recurrent bullous dermatitis artefacta mimicking immunobullous disease
Authors: R.M. Azurdia, D.M. Guerin, G.R. Sharpe
Journal: British Journal of Dermatology (2000)

SIR, Dermatitis artefacta can mimic a number of common skin disorders. We present an example of an unusual and treatment‐resistant blistering disorder in an adolescent girl which led to a delay in the diagnosis of dermatitis artefacta. An 11‐year‐old girl presented in 1997 with a 2‐week history of a blistering rash on the dorsa of the hands and forearms. She was normally fit and well with no preceding history of skin disease. She was the youngest of four girls and lived at home with her parents. The rash was initially diagnosed and treated as bullous impetigo but blistering continued at these sites for several weeks, despite antibiotics and with negative cultures. Skin biopsy showed necrosis of the full thickness of the epidermis, and a diagnosis of erythema multiforme was suggested. The blistering settled after several months but 16 months later she was urgently referred back to the clinic when further tense blisters had appeared overnight. There was scarring of the skin but mucosae and conjunctivae were normal. A second skin biopsy showed similar full‐thickness necrosis of the epidermis; direct immunofluorescence was negative for fibrinogen, complement C3, IgG, IgA and IgM. Immunological investigation showed positive antinuclear and anti‐Sm antibody titres at 1 : 64, and complement levels were low. Bullous lupus erythematosus was considered a possible diagnosis, despite the negative immunofluorescence. Systemic steroids and dapsone were commenced, but without improvement. At a subsequent visit, a large tense blister with a sharply defined straight edge of erythema was apparent on her arm (Fig. 1a) and over the dorsal aspect of her foot. A diagnosis of dermatitis artefacta was suspected and the medications withdrawn. A third skin biopsy showed a subepidermal separation of totally necrotic epidermis, creating a cell‐free blister. The adjacent epidermis showed basal cell liquefactive degeneration, disorderly maturation and multinucleate pleomorphic keratinocytes (Fig. 1b). The appearances were unusual, suggesting the possibility of an exogenous agent. Several aerosols and cosmetics were removed from her possession while in hospital and the diagnosis was discussed with the patient and her parents separately. The blisters all healed rapidly and 12 months later, blistering had ceased and she had returned to school.
Nutrition Therapy Recommendations for the Management of Adults With Diabetes
Authors: Alison B. Evert, Jackie L. Boucher, Marjorie Cypress, Stephanie A. Dunbar, Marion J. Franz, Elizabeth J. Mayer-Davis, Joshua J. Neumiller, Robin Nwankwo, Cassandra L. Verdi, Patti Urbanski, William S. Yancy
Journal: Diabetes Care (2013)

There is no standard meal plan or eating pattern that works universally for all people with diabetes. In order to be effective, nutrition therapy should be individualized for each patient/client based on his or her individual health goals; personal and cultural preferences; health literacy and numeracy; access to healthful choices; and readiness, willingness, and ability to change. Nutrition interventions should emphasize a variety of minimally processed nutrient dense foods in appropriate portion sizes as part of a healthful eating pattern and provide the individual with diabetes with practical tools for day-to-day food plan and behavior change that can be maintained over the long term.
Degree of synovitis on MRI is correlated with histological and macroscopic features of synovial tissue inflammation in knee osteoarthritis
Authors: B J E de Lange-Brokaar, A Ioan-Facsinay, A W Visser, S N Andersen, L van Toorn, G J V M van Osch, A-M Zuurmond, V Stojanovic-Susulic, M Reijnierse, R G H H Nelissen, T W Huizinga, M Kloppenburg
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background and objectives</h3> Synovitis is often present on MRI of OA knees and is an important determinant of pain. To better understand the nature of synovitis seen on MRI the authors compared microscopic and macroscopic features of synovial tissue inflammation with synovitis grade on contrast enhanced (CE) MRI. <h3>Methods and methods</h3> Twenty-two patients (mean age 61±7 years, 73% women, mean BMI 30±5 kg/mm2) with symptomatic radiographic knee OA attending the rheumatology outpatient clinic were included. Arthroscopy of the index knee was performed and macroscopic features (neovascularisation, villi, fibrin and hyperplasia) were scored (0–4). Furthermore, 15–20 synovial biopsies per knee were obtained. After H&amp;E staining, synovial tissue samples were microscopically scored on features: synovial lining layer hyperplasia/enlargement, activation of resident cells/stroma and degree of inflammatory infiltrates. Each feature was scored from 0–3 and a total sum score per patient was devised. Mean total scores (0–9) by three observers were used. Saggital and axial T1-weighted CE MRI images (3T) were used to semi quantitatively score synovitis at 11 different sites according to Guermazi <i>et al</i>, ranging from 0–22.1 Self reported pain was assessed by visual analogue scale (VAS, 0–100). Pearson correlations adjusted for age were used for correlation between total histology synovitis score and total MRI score. Spearman ρ correlations were used for correlation between total histology score and macroscopic features. Both were calculated by SPSS 16.0. <h3>Results</h3> The mean (SD) synovitis score on MRI was 7.8 (3.9), representing a mild synovitis and mean (SD) histology score was 2.1 (1.5). Median (range) score of macroscopic features (0–4) were 2.0 (1.0–4.0) for neovascularisation, 1.0 (0.0–3.0) for hyperplasia, 2.0 (0.0–4.0) for villi and 2.0 (0.0–3.0) for fibrin. Synovitis score on MRI correlated significantly with microscopic synovitis score (r=0.5, p=0.019] and macroscopic neovascularisation score (r=0.6, p=0.002) and hyperplasia (r=0.4, p=0.40). Furthermore statistically significant correlation between microscopic synovitis score and macroscopic neovascularisation (r=0.5, p=0.012) existed. No significant correlations with VAS pain were seen. <h3>Conclusions</h3> Synovitis severity on T1 weighted CE MRI images is significantly correlated with both macroscopic and microscopic features of synovitis in patients with knee OA. No association with severity of pain was seen. Therefore, CE MRI evaluation is a reliable, non invasive way to determine synovitis severity in OA patients.
Nonsteroidal Anti-inflammatory Drug Use After 3 Years of Aspirin Use and Colorectal Adenoma Risk: Observational Follow-up of a Randomized Study
Authors: Maria V. Grau, Robert S. Sandler, Gail McKeown-Eyssen, Robert S. Bresalier, Robert W. Haile, Elizabeth L. Barry, Dennis J. Ahnen, Jiang Gui, Robert W. Summers, John A. Baron
Journal: JNCI Journal of the National Cancer Institute (2009)

Frequent use of nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to reduce the risk of colorectal adenomas in randomized trials. We examined the persistence of the protective effect after the cessation of randomized aspirin treatment and whether it is affected by the duration and frequency of subsequent NSAID use.We used data from the Aspirin/Folate Polyp Prevention Study (AFPPS), in which 1121 subjects were randomly assigned to receive placebo or aspirin (81 or 325 mg/d) for 3 years. After the end of treatment and a follow-up colonoscopy, AFPPS participants were invited to remain under follow-up until their next surveillance colonoscopies, scheduled 3-5 years later. Information regarding use of NSAIDs during posttreatment follow-up was gathered periodically via questionnaires. Average weekly NSAID use was classified as sporadic (<2 days per week), moderate (2 to <4 days per week), or frequent (>or=4 days per week). The analysis was stratified according to randomized aspirin groups and posttreatment NSAID use; placebo subjects who later were sporadic NSAID users formed the reference group. The primary outcomes were all adenomas and advanced lesions. Adjusted relative risks and 95% confidence intervals were computed with generalized linear models. All statistical tests were two-sided.A total of 850 subjects underwent a posttreatment colonoscopy, on average 4 years after the end of study treatment. The protective effect of 81 mg of aspirin for colorectal adenomas persisted with continued posttreatment NSAID use. The risk of any adenoma among frequent NSAID users was 26.8% vs 39.9% among placebo subjects who later used NSAIDs sporadically (adjusted relative risk = 0.62, 95% confidence interval [CI] = 0.39 to 0.98; P(trend) with NSAID use frequency = .03). The unadjusted absolute risk reduction was 13.1 percentage points (95% CI = -0.3 to 26.5 percentage points) (P = .07). Results for 325 mg of aspirin were similar, although not statistically significant. For advanced lesions, small numbers of endpoints limited the analysis, but findings among subjects randomly assigned to 81 mg of aspirin suggested a protective association regardless of posttreatment NSAID use.Long-term and frequent use of NSAIDs may enhance the chemopreventive effect of aspirin against colorectal neoplasia.
Natural anticoagulants limit lipopolysaccharide-induced pulmonary coagulation but not inflammation
Authors: G. Choi, A. P. J. Vlaar, M. Schouten, C. van't Veer, T. van der Poll, M. Levi, M. J. Schultz
Journal: European Respiratory Journal (2007)

Pulmonary coagulopathy and hyperinflammation may contribute to an adverse outcome in sepsis. The present study determines the effects of natural inhibitors of coagulation on bronchoalveolar haemostasis and inflammation in a rat model of endotoxaemia. Male Sprague-Dawley rats were randomised to treatment with normal saline, recombinant human activated protein C (APC), plasma-derived antithrombin (AT), recombinant human tissue factor pathway inhibitor (TFPI), heparin or recombinant tissue plasminogen activator (tPA). Rats were intravenously injected with lipopolysaccharide (LPS), which induced a systemic inflammatory response and pulmonary inflammation. Blood and bronchoalveolar lavage were obtained at 4 and 16 h after LPS injection, and markers of coagulation and inflammation were measured. LPS injection caused an increase in the levels of thrombin–AT complexes, whereas plasminogen activator activity was attenuated, both systemically and within the bronchoalveolar compartment. Administration of APC, AT and TFPI significantly limited LPS-induced generation of thrombin–AT complexes in the lungs, and tPA stimulated pulmonary fibrinolytic activity. However, none of the agents had significant effects on the production of pulmonary cytokines, chemokines, neutrophil influx and myeloperoxidase activity. Natural inhibitors of coagulation prevent bronchoalveolar activation of coagulation, but do not induce major alterations of the pulmonary inflammatory response in rat endotoxaemia.
Benzo[a]pyrene Diol Epoxide and Bleomycin Sensitivity and Susceptibility to Cancer of Upper Aerodigestive Tract
Authors: X Wu, J Gu, W K Hong, J J Lee, C I Amos, H Jiang, R J Winn, K K Fu, J Cooper, M R Spitz
Journal: JNCI Journal of the National Cancer Institute (1998)

Background: Tobacco smoking is an established risk factor for cancers of the upper aerodigestive tract, and measurement of chromosomal aberrations, i.e., chromatid breaks, induced in lymphocytes in vitro by bleomycin has been shown to be a predictor of risk for these cancers. In a case-control study, we recruited case subjects who were previously treated with surgery and/or radiotherapy for stage I or stage II squamous cell carcinoma of the head and neck to test the hypothesis that lymphocytic chromatid breaks induced by benzo[a]pyrene diol epoxide (BPDE), a tobacco mutagen, may also be associated with risk of developing cancers of the upper aerodigestive tract. Methods: Case subjects were matched to control subjects on the basis of age, sex, ethnicity, and smoking status. Primary lymphocytes from 67 case subjects and 81 control subjects were treated with 2 iM BPDE for 24 hours, and the frequency of induced chromatid breaks was determined. All statistical tests were two-sided. Results: Lymphocytes from case subjects compared with lymphocytes from control subjects showed significantly more breaks per cell induced by BPDE (mean ± standard deviation, 0.77 ± 0.38 versus 0.49 ± 0.25; P<.001). Lymphocytes from 64.2% of case subjects were sensitive to BPDE (using a cutoff value of >0.60 break per cell). Subjects in the highest quartile of chromatid breaks had an approximately 20-fold increased risk of cancer compared with those in the lowest quartile after adjustment for age, sex, ethnicity, and smoking status. The association between BPDE sensitivity and cancer risk was higher in former smokers than in current smokers and higher in younger patients than in older patients. Subjects with sensitivity to both BPDE and bleomycin were at a 19.2-fold increased risk of cancer compared with those who were not sensitive to either agent. Conclusions: Mutagen sensitivity assays may aid in identifying individuals at risk of cancer, and use of parallel assays with two mutagens may improve risk predictability. [J Natl Cancer Inst 1998;90:1393-9]
Is a Complete Remission of Intestinal Metaplasia a Suitable Endpoint in Patients Undergoing Radiofrequency Ablation (RFA)? Long-Term Results of RFA Treatment in 62 Consecutive Patients
Authors: Krajciova Jana, Stefanova Magdalena, Maluskova Jana, Kollar Marek, Spicak Julius, Martinek Jan
Journal: Annals of Oncology (2014)
The histamine H<sub>4</sub> receptor mediates inflammation and Th17 responses in preclinical models of arthritis
Authors: Jeffery M Cowden, Fuqu Yu, Homayon Banie, Mandana Farahani, Ping Ling, Steven Nguyen, Jason P Riley, Mai Zhang, Jian Zhu, Paul J Dunford, Robin L Thurmond
Journal: Annals of the Rheumatic Diseases (2013)

The histamine H4 receptor (H4R) has been shown to drive inflammatory responses in models of asthma, colitis and dermatitis, and in these models it appears to affect both innate and adaptive immune responses. In this study, we used both H4R-deficient mice and a specific H4R antagonist, JNJ 28307474, to investigate the involvement of the H4R in mouse arthritis models.H4R-deficient mice and wild-type mice administered the H4R antagonist were studied in models of collagen antibody-induced arthritis (CAIA) and collagen-induced arthritis (CIA). The impact on Th17 cells was assessed by restimulation of inguinal lymphocytes in the disease or immunisation models and with in vitro stimulation of whole blood.Both H4R-deficient mice and mice treated with the H4R antagonist exhibited reduced arthritis disease severity in both CAIA and CIA models. This was evident from the reduction in disease score and in joint histology. In the CIA model, treatment with the H4R antagonist reduced the number of interleukin (IL)-17 positive cells in the lymph node and the total production of IL-17. Th17 cell development in vivo was reduced in H4R-deficient mice or in mice treated with an H4R antagonist. Finally, treatment of both mouse and human blood with an H4R antagonist reduced the production of IL-17 when cells were stimulated in vitro.These results implicate the H4R in disease progression in arthritis and in the production of IL-17 from Th17 cells. This work supports future clinical exploration of H4R antagonists for the treatment of rheumatoid arthritis.