tbuckley/cabot-search huggingface dataset:
Physical activity attenuates fluid shift and obstructive sleep apnea
Authors: Stefania Redolfi, Nicola Venturoli, Marco Ravanelli, Luigi Taranto-Montemurro, Michela Bettinzoli, Luciano Corda, Leonardo Pedroni, Thomas Similowski, Claudio Tantucci
Journal: European Respiratory Journal (2013)

RATIONALE  Exercise attenuates obstructive sleep apnea (OSA) without weight loss, but the underlying mechanisms remain unknown. Sedentary living promotes fluid accumulation in the legs, which is counteracted by physical activity. We have previously shown that prevention of daytime fluid accumulation in the legs and its nocturnal shift into the neck, reduces the number of apneas and hypopneas per hour of sleep (AHI). We hypothesized that, in sedentary men with OSA, physical activity will reduce the AHI by decreasing the nocturnal fluid shift into the neck.   METHODS  Sedentary men with OSA were randomly assigned to one-week of physical activity (2 time/day of 45 min of moderate walk) or to one-week control period without physical activity, after which they crossed over to the other arm. Polysomnography, measurement of nocturnal changes in leg fluid volume, in neck circumference and in upper airway (UA) air volume by magnetic resonance imaging (MRI) were performed at the end of the exercise and control periods.   RESULTS  We enrolled 6 men (age 56±13 yrs; BMI 28.2±4.9). Compared to the end of the control period, at the end of the exercise period there was a 40% reduction in the nocturnal leg fluid shift ( P =0.012) and a 70% reduction in the nocturnal neck enlargement ( P =0.033) in association with a 21% reduction in the AHI (from 60.9±33.4 to 44.1±23.4,  P =0.019). MRI showed a nocturnal 12% reduction in the UA air volume ( P =0.025) at the end of the control period and no change at the end of the exercise period.   CONCLUSIONS  We suggest that exercise attenuates OSA by counteracting daytime fluid accumulation in the legs and overnight fluid redistribution into the neck around UA, preventing UA air volume reduction during sleep.
Dietary Fat Intake and Endogenous Sex Steroid Hormone Levels in Postmenopausal Women
Authors: Michelle D. Holmes, Donna Spiegelman, Walter C. Willett, JoAnn E. Manson, David J. Hunter, Robert L. Barbieri, Graham A. Colditz, Susan E. Hankinson
Journal: Journal of Clinical Oncology (2000)

PURPOSE: To examine the relationship between plasma levels of reproductive sex steroid hormones in postmenopausal women and their reported fat intake. METHODS: We measured plasma sex steroid hormones levels in plasma collected in 1989 and 1990 from 381 healthy postmenopausal women. For each woman, we measured fat intake in 1986 and 1990 by a food-frequency questionnaire. The cross-sectional associations between the percentage of energy from total and specific types of dietary fat intake and plasma hormone levels were assessed by linear regression, controlling for energy intake, obesity, and protein intake. RESULTS: The plasma estradiol level was 4.3% lower (95% confidence limits, −8.3%, −0.2%) for a substitution of 5% of energy from fat intake for an equivalent amount of energy from carbohydrate when adjusted for obesity and other covariates. Estradiol was also inversely associated with all other fat types except trans fat; the inverse associations with vegetable fat and marine omega-3 fats were statistically significant. CONCLUSION: We observed an inverse association between total fat intake averaged over 4 to 5 years and estradiol levels. This result is inconsistent with the hypothesis that fat intake predisposes to breast cancer risk by raising endogenous estrogen levels.
IL17 Promotes Mammary Tumor Progression by Changing the Behavior of Tumor Cells and Eliciting Tumorigenic Neutrophils Recruitment
Authors: Luciana Benevides, Denise Morais da Fonseca, Paula Barbim Donate, Daniel Guimarães Tiezzi, Daniel D. De Carvalho, Jurandyr M. de Andrade, Gislaine A. Martins, João S. Silva
Journal: Cancer Research (2015)

The aggressiveness of invasive ductal carcinoma (IDC) of the breast is associated with increased IL17 levels. Studying the role of IL17 in invasive breast tumor pathogenesis, we found that metastatic primary tumor-infiltrating T lymphocytes produced elevated levels of IL17, whereas IL17 neutralization inhibited tumor growth and prevented the migration of neutrophils and tumor cells to secondary disease sites. Tumorigenic neutrophils promote disease progression, producing CXCL1, MMP9, VEGF, and TNFα, and their depletion suppressed tumor growth. IL17A also induced IL6 and CCL20 production in metastatic tumor cells, favoring the recruitment and differentiation of Th17. In addition, IL17A changed the gene-expression profile and the behavior of nonmetastatic tumor cells, causing tumor growth in vivo, confirming the protumor role of IL17. Furthermore, high IL17 expression was associated with lower disease-free survival and worse prognosis in IDC patients. Thus, IL17 blockade represents an attractive approach for the control of invasive breast tumors.
Synovial tissue volume: a treatment target in knee osteoarthritis (OA)
Authors: Terence W O'Neill, Matthew J Parkes, Nasimah Maricar, Elizabeth J Marjanovic, Richard Hodgson, Andrew D Gait, Timothy F Cootes, Charles E Hutchinson, David T Felson
Journal: Annals of the Rheumatic Diseases (2015)

Synovitis occurring frequently in osteoarthritis (OA) may be a targeted outcome. There are no data examining whether synovitis changes following intra-articular intervention.Persons aged 40 years and older with painful knee OA participated in an open label trial of intra-articular steroid therapy. At all time points they completed the Knee Injury and Osteoarthritis Outcome Score (KOOS) questionnaire. They had a contrast-enhanced (CE) MRI immediately prior to an intra-articular steroid injection with a repeat scan within 20 days. Response status was assessed using the Osteoarthritis Research Society International (OARSI) response criteria. OARSI responders were followed until their pain relapsed either within 20% of baseline or 6 months, shortly after which a third MRI was performed. Synovial tissue volume (STV) was measured on postcontrast knee images. We looked at changes in the STV and in pain, and their association.120 subjects with preinjection and postinjection CE MRI were followed. Their mean age was 62.3 years (SD=10.3) and 62 (52%) were women. The median time between injection and follow-up scan was 8 days (IQR 7-14 days). 85/120 (71%) were OARSI responders. Pain decreased (mean change in KOOS=+23.9; 95% CI 20.1 to 27.8, p<0.001) following steroid injection, as did mean STV (mean change=-1071 mm(3); 95% CI -1839 mm(3) to -303 mm(3), p=0.01). Of the 80 who returned for a third MRI, pain relapsed in 57, and in the 48 of those with MRI data, STV increased between follow-up and final visit (+1220 mm(3); 95% CI 25 mm(3) to 2414 mm(3), p=0.05). 23 were persistent responders at 6 months and, in these, STV did not increase (mean change=-202 mm(3); 95% CI -2008 mm(3) to 1604 mm(3), p=0.83). Controlling for variation over time, there was a significant association between synovitis volume and KOOS pain (b coefficient-change in KOOS pain score per 1000 mm(3) change in STV=-1.13; 95% CI -1.87 to -0.39, p=0.003), although STV accounted for only a small proportion of the variance in change in pain.Synovial tissue volume in knee OA shrinks following steroid therapy, and rebounds in those whose pain relapses. It can be considered a treatment target in symptomatic knee OA.ISRCTN07329370.
High-dose induction chemotherapy with cyclophosphamide, etoposide, and cisplatin for extensive-stage small-cell lung cancer.
Authors: D H Johnson, M J DeLeo, K R Hande, S N Wolff, J D Hainsworth, F A Greco
Journal: Journal of Clinical Oncology (1987)

To exploit possible dose-response and combination drug synergism, 20 previously untreated patients with extensive-stage small-cell lung cancer (SCLC) received one or two courses of high-dose induction chemotherapy consisting of cyclophosphamide (100 mg/kg), etoposide (1,200 mg/m2), and cisplatin (120 mg/m2) (HDCEP). HDCEP was followed by four cycles of standard-dose cyclophosphamide (1,000 mg/m2), doxorubicin (40 mg/m2), and vincristine (1.4 mg/m2) (CAV). Response was determined after HDCEP and following CAV. Reevaluation included repeat bronchoscopy and chest computerized tomography (CT), as well as repetition of all initially abnormal studies. All patients were evaluable for response and toxicity. Overall response to HDCEP was 90%, with a complete response (CR) rate of 65% (95% confidence limits, 44% to 86%) and a partial response (PR) rate of 25% (95% confidence limits, 6% to 44%). All patients either maintained or improved their initial response while receiving CAV. Median duration of response was 6 months (range, 2 to 12 months) and median survival was 9.5 + months (range, 2 to 21 + months). All 37 courses of HDCEP were associated with leukopenia (less than 1,000/microL), 92% with thrombocytopenia (less than 20,000/microL), and 84% with fever of greater than 38.5 degrees C. Additional toxicities included bacteremia (24%), nausea and emesis (59%), mucositis (57%), diarrhea (38%), and hemorrhagic cystitis (5%). There were two treatment-related deaths due to infection. A third patient died 4 months after completing HDCEP with pulmonary fibrosis. Although response duration and median survival were not improved, HDCEP produced a high CR rate in ambulatory patients with extensive-stage SCLC.
Pig-tail drainage for primary spontaneous pneumothorax: dose the position influence the treatment result
Authors: 陳煒(Wei Chen), 杭良文(Liang Wen Hang), 夏德椿(Te Chun Hsia), 施純明(Chuen Ming Shih), 徐武輝(Wu Huei Hsu)
Journal: European Respiratory Journal (2005)
Renal Tumors in Mice: Light Microscopic Observations of Epithelial Tumors Induced by Ethylnitrosourea&lt;xref ref-type="fn" rid="fn2"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: L S Lombard, J M Rice, S D Vesselinovitch
Journal: JNCI Journal of the National Cancer Institute (1974)

Renal epithelial tumors developing in (C3HeB/FeJ × A/J)F1 and (C57BL/6J × C3HeB/FeJ)F1 mice after a single postnatal injection of l-ethyl-l-nitrosourea (ENU) are described. Most of these neoplasms were benign and resembled the corresponding human renal adenomas in morphology and biologic behavior. Three morphologic variants were distinguished by papillary cystic, platelike, or tubular patterns of growth. Most adenomas had a papillary cystadenomatous architecture and about a third were bilateral. Malignancy was not evident from this common morphologic variant, though some papillary cystadenomas reached dimensions greater than those of the normal kidney. In contrast, pulmonary metastases were observed from both tubular and platelike granular or “clear-cell” neoplasms. Hyperplasia ot the proximal convoluted tubular epithelium with or without cystic dilatation of the tubule and infoldings of the epithelium was recognized as a preneoplastic lesion. Morphologic and staining characteristics of cells from early microscopic lesions indicated that both papillary cystic and solid-cell tumors originated from proximal convoluted tubular epithelium.
Heart and heart-lung transplantation in Down's syndrome
Authors: H. Leonard
Journal: BMJ (2000)

Congenital heart disease is common in Down's syndrome, occurring in about 40% of individuals.1 Twenty years ago cardiac surgery was often not attempted in children with Down's syndrome because of operative mortality of up to 60% and a short life expectancy.2 With improvements in paediatric cardiac surgery and changes in attitude towards children with Down's syndrome such children now undergo corrective cardiac surgery. Some will inevitably develop complications and may benefit from heart transplant. There is also a large group of young adults with Down's syndrome who did not have heart surgery when young and who have uncorrected heart lesions that are now inoperable because of irreversible pulmonary vascular disease. They too are potential candidates for heart-lung transplantation. There is no published literature on heart or heart-lung transplantation in Down's syndrome, which makes it hard to predict the outcome in these patients.

Heart transplantation is now a widely accepted treatment, and medium term survival has steadily improved.3 The results of heart-lung transplantation are not as good but have …
Serotypes and clinical manifestations of invasive group B streptococcal infections in western Sweden 1998-2001
Authors: E. Persson, S. Berg, B. Trollfors, P. Larsson, E. Ek, E. Backhaus, B.E.B. Claesson, L. Jonsson, G. Rådberg, T. Ripa, S. Johansson
Journal: Clinical Microbiology and Infection (2004)
Smoker's Lung Transplanted to a Nonsmoker
Authors: LEILA JOHN MARQUES, HELMUT TESCHLER, JOSUNE GUZMAN, ULRICH COSTABEL
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

Alveolar macrophages (AM) from smokers contain characteristic smoker's inclusion bodies within the cytoplasm as a result of ingestion of substances in the inhaled smoke. How long these smoking-related changes in the AM population can be seen after smoking cessation is largely unknown. We had the unique opportunity to investigate a 51-yr-old never-smoker after single lung transplantation (TX) for alpha 1-antitrypsin deficiency emphysema who received a donor's lung from a heavy cigarette smoker. Serial bronchoalveolar lavage (BAL) was performed in the donor's lung for transplant surveillance at defined time intervals, and the percentage of AM with characteristic smoker's inclusions was counted on slides stained with May-Grünwald-Giemsa stain. The patient had an uneventful course after TX with no major infectious complications or episodes of rejection. One month after TX the percentage of smoker's AM was 98%. BAL after 2, 5, 7, and 12 mo showed a similar high percentage. After 18 mo a first a decrease was seen, down to 78%, and after 2 yr a decrease to 59% was seen. After 3 yr, the smoker's AM had mostly disappeared, only 3% were still present. In conclusion, smoker's inclusions in AM may be detected for at least 2 yr after smoking has ceased, which is considerably longer than the estimated life span of the AM.
Dual prognostic significance of tumour-associated macrophages in human pancreatic adenocarcinoma treated or untreated with chemotherapy
Authors: Giuseppe Di Caro, Nina Cortese, Giovanni Francesco Castino, Fabio Grizzi, Francesca Gavazzi, Cristina Ridolfi, Giovanni Capretti, Rossana Mineri, Jelena Todoric, Alessandro Zerbi, Paola Allavena, Alberto Mantovani, Federica Marchesi
Journal: Gut (2015)

Tumour-associated macrophages (TAMs) play key roles in tumour progression. Recent evidence suggests that TAMs critically modulate the efficacy of anticancer therapies, raising the prospect of their targeting in human cancer.In a large retrospective cohort study involving 110 patients with pancreatic ductal adenocarcinoma (PDAC), we assessed the density of CD68-TAM immune reactive area (%IRA) at the tumour-stroma interface and addressed their prognostic relevance in relation to postsurgical adjuvant chemotherapy (CTX). In vitro, we dissected the synergism of CTX and TAMs.In human PDAC, TAMs predominantly exhibited an immunoregulatory profile, characterised by expression of scavenger receptors (CD206, CD163) and production of interleukin 10 (IL-10). Surprisingly, while the density of TAMs associated to worse prognosis and distant metastasis, CTX restrained their protumour prognostic significance. High density of TAMs at the tumour-stroma interface positively dictated prognostic responsiveness to CTX independently of T-cell density. Accordingly, in vitro, gemcitabine-treated macrophages became tumoricidal, activating a cytotoxic gene expression programme, inhibiting their protumoural effect and switching to an antitumour phenotype. In patients with human PDAC, neoadjuvant CTX was associated to a decreased density of CD206(+) and IL-10(+) TAMs at the tumour-stroma interface.Overall, our data highlight TAMs as critical determinants of prognostic responsiveness to CTX and provide clinical and in vitro evidence that CTX overall directly re-educates TAMs to restrain tumour progression. These results suggest that the quantification of TAMs could be exploited to select patients more likely to respond to CTX and provide the basis for novel strategies aimed at re-educating macrophages in the context of CTX.
Phenotype of Normal Spirometry in an Aging Population
Authors: Carlos A. Vaz Fragoso, Gail McAvay, Peter H. Van Ness, Richard Casaburi, Robert L. Jensen, Neil MacIntyre, Thomas M. Gill, H. Klar Yaggi, John Concato
Journal: American Journal of Respiratory and Critical Care Medicine (2015)

Rationale: In aging populations, the commonly used Global Initiative for Chronic Obstructive Lung Disease (GOLD) may misclassify normal spirometry as respiratory impairment (airflow obstruction and restrictive pattern), including the presumption of respiratory disease (chronic obstructive pulmonary disease [COPD]).Objectives: To evaluate the phenotype of normal spirometry as defined by a new approach from the Global Lung Initiative (GLI), overall and across GOLD spirometric categories.Methods: Using data from COPDGene (n = 10,131; ages 45–81; smoking history, ≥10 pack-years), we evaluated spirometry and multiple phenotypes, including dyspnea severity (Modified Medical Research Council grade 0–4), health-related quality of life (St. George's Respiratory Questionnaire total score), 6-minute-walk distance, bronchodilator reversibility (FEV1 % change), computed tomography–measured percentage of lung with emphysema (% emphysema) and gas trapping (% gas trapping), and small airway dimensions (square root of the wall area for a standardized airway with an internal perimeter of 10 mm).Measurements and Main Results: Among 5,100 participants with GLI-defined normal spirometry, GOLD identified respiratory impairment in 1,146 (22.5%), including a restrictive pattern in 464 (9.1%), mild COPD in 380 (7.5%), moderate COPD in 302 (5.9%), and severe COPD in none. Overall, the phenotype of GLI-defined normal spirometry included normal adjusted mean values for dyspnea grade (0.8), St. George's Respiratory Questionnaire (15.9), 6-minute-walk distance (1,424 ft [434 m]), bronchodilator reversibility (2.7%), % emphysema (0.9%), % gas trapping (10.7%), and square root of the wall area for a standardized airway with an internal perimeter of 10 mm (3.65 mm); corresponding 95% confidence intervals were similarly normal. These phenotypes remained normal for GLI-defined normal spirometry across GOLD spirometric categories.Conclusions: GLI-defined normal spirometry, even when classified as respiratory impairment by GOLD, included adjusted mean values in the normal range for multiple phenotypes. These results suggest that among adults with GLI-defined normal spirometry, GOLD may misclassify normal phenotypes as having respiratory impairment.
Etiologic Relationship of Skin Tumors (Skin Leukosis) of Chickens to Marek's Disease<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref><xref ref-type="fn" rid="FN4">4</xref>
Authors: J. M. Sharma, W. C. Davis, S. G. Kenzy
Journal: JNCI Journal of the National Cancer Institute (1970)
The induction of experimental autoimmune myocarditis in mice lacking CD4 or CD8 molecules [corrected]
Authors: J M Penninger, N Neu, E Timms, V A Wallace, D R Koh, K Kishihara, C Pummerer, T W Mak
Journal: The Journal of Experimental Medicine (1993)

Experimental induction of most autoimmune diseases appears to depend on the activation of CD4+ T helper cells, while CD8+ lymphocytes may have a role in disease progression. To study the role of CD4+ and CD8+ T cell subsets in T cell-dependent autoimmunity, mice lacking CD4 or CD8 molecules after gene targeting were injected with cardiac myosin to induce organ specific autoimmune myocarditis. Mice homozygous for the CD8 mutation (CD8-/-) developed significantly more severe disease as compared to CD4+/-CD8+/- controls. Surprisingly, CD4-/- mice developed autoimmune myocarditis with infiltration of TCR alpha beta +CD4-CD8- T cells in the heart tissue and appearance of autoantibodies. These data demonstrate that the lack of CD4+ or CD8+ T cells has no significant influence on the initiation of autoimmune myocarditis. CD4+ and CD8+ cells regulate disease severity and these results may explain the occurrence of autoimmunity in CD4 immunodeficiencies.
Responsiveness of Carcinogen-Induced Hyperplastic Alveolar Nodules in Lewis Rats to Mammary Gland Growth-Regulatory Mechanisms&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: Leonard J. Beuving
Journal: JNCI Journal of the National Cancer Institute (1969)

When tested by the mammary fat-pad transplantation technique, hyperactive outgrowths derived from preneoplastic, carcinogen-induced, hyperplastic alveolar nodules in rats were as responsive to mammary gland growth-regulatory mechanisms as normal mammary epithelial elements. Preneoplastic lesions produced neither outgrowths nor tumors when transplanted into subcutaneous connective tissue or intact mammary glands. On the other hand, transplantable, primary mammary adenocarcinomas from carcinogen-treated rats grew progressively in gland-free mammary fat pads, mammary glands, and subcutaneous connective tissue. Accordingly, the preneoplastic lesions more closely resemble normal mammary epithelial elements than mammary tumors in these distinguishing biologic characteristics, and the behavior of these lesions from the rat mammary gland is similar to that of the hyperplastic alveolar nodules of the mouse.
Recombination of B7-H4 and CD68 predicted lymph node metastasis in human lung carcinoma
Authors: Jian An Huang, Cheng Chen
Journal: European Respiratory Journal (2013)

Background:  B7-H4 (also called B7S1 and B7x) is the most recent addition to the B7 family. Putative receptor of B7-H4 can be unregulated on activated T cells. By the cell cycle, B7-H4 ligation of T cells has a profound inhibitory effect on the growth, cytokine secretion, and development of cytotoxicity. The observations suggest that B7-H4 over-expression may reflect a more aggressive biologic potential and may play a role in tumor immune surveillance mechanisms.   Objective:  To study the expression of negative costimulatroy molecule B7-H4 in non-small cell lung cancer (NSCLC)tissues and its relationship with the clinical features of NSCLC.   Method:  B7-H4 expression and infiltration of CD8 T cells and CD68 cells in NSCLC tissues were detected by immunohistoehemistry. The correlation between B7-H4 expression and CD68 cells was studied.   Result:  The positive rate of B7-H4 in 52 NSCLC tissues was 45.76%%. B7-H4 expression was positively correlated with the clinical tumor stages and lymph node metastasis of NSCLC and CD68 cells, negatively correlated with tumor infiltration of CD8 T cells. Combining detection of B7-H4 and CD68 expression in lung carcinoma tissues can offer a valuable reference to evaluate the lymph node metastasis.   Conclusion:  It is evident that B7-H4 is overexpressed in NSCLC, and it plays certain role in oncogenesis and progression of human NSCLC.