tbuckley/cabot-search huggingface dataset:
Abstract 3966: Absence of Macrophage Mcl-1 Induces Foam Cell Formation and Atherosclerotic Plaque Apoptosis without Affecting Plaque Development in LDLr-/- Mice
Authors: Marijke M Westra, Ilze Bot, Ivan Dzhagalov, You-Wen He, Theo J van Berkel, Erik A Biessen
Journal: Circulation (2008)

Anti-apoptotic Bcl-2 family member myeloid cell leukemia 1 (Mcl-1) plays an important, in neutrophils essential, role in promoting survival and differentiation of leukocyte subsets. Mcl-1 was shown...
The LincRNA HOTAIRM1, Located in the HOXA genomic Region, impacts Prognosis in Acute Myeloid Leukemia and Is Associated with a Distinctive microRNA Signature
Authors: Marina Díaz-Beyá, Alfons Navarro, Salut Brunet, Josep F Nomdedeu, Anna Cordeiro, Marta Pratcorona, Meritxell Nomdedeu, Ruth M Risueño, Josep-Maria Ribera, Mar Tormo, Rafael F. Duarte, Olga Salamero, Lourdes Escoda, David Gallardo, Carmen Pedro, Josep M Marti-Tutusaus, Jorge Sierra, Mariano Monzó, Jordi Esteve
Journal: Blood (2014)
Memory Impairment in Schizophrenia: A Meta-Analysis
Authors: André Aleman, Ron Hijman, Edward H.F. de Haan, René S. Kahn
Journal: American Journal of Psychiatry (1999)

Memory impairment is well documented in schizophrenia. Less is known, however, about the exact magnitude, pattern, and extent of the impairment. The effect of potential moderator variables, such as medication status and duration of illness, is also unclear. In this article, the authors presented meta-analyses of the published literature on recall and recognition memory performance between patients with schizophrenia and normal comparison subjects.Meta-analyses were conducted on 70 studies that reported measures of long-term memory (free recall, cued recall, and recognition of verbal and nonverbal material) and short-term memory (digit span). Tests of categorical models were used in analyses of potential moderators (clinical variables and study characteristics).The findings revealed a significant and stable association between schizophrenia and memory impairment. The composite effect size for recall performance was large. Recognition showed less, but still significant, impairment. The magnitude of memory impairment was not affected by age, medication, duration of illness, patient status, severity of psychopathology, or positive symptoms. Negative symptoms showed a small but significant relation with memory impairment.This meta-analysis documented significant memory impairment in schizophrenia. The impairment was stable, wide ranging, and not substantially affected by potential moderating factors such as severity of psychopathology and duration of illness.
G-Banding Patterns in Mouse Lymphoblastic Leukemia L1210
Authors: K Dowjat, I Włodarska
Journal: JNCI Journal of the National Cancer Institute (1981)

The karyotype of murine lymphoblastic leukemia L1210 was studied with the use of the trypsin-Giemsa technique. The line was hypodiploid with a modal number of 38 chromosomes, including three biarmed chromosomes. All cells examined contained at least one copy of each normal chromosome with the exception of chromosome #1. in which a whole copy along with parts of the second copy was found in the marker chromosome's composition. In 65% of the cells, trisomy of chromosome #15 was observed. Nearly all cells contained only one X chromosome. The 13 marker chromosomes that frequently occurred are described. and the presumed origin of seven of these chromosomes is described in detail. Comparison of the karyotype of murine L1210 leukemia with the karyotypes of other leukemias of the mouse showed the existence of similar chromosome aberrations. Among these aberrations. the trisomy of chromosome #15 and monosomy of the X-chromosome may be of special importance. The possible role of karyotypic changes in the genesis of the malignant phenotype of the cells is discussed.
Assessment of impaired in vitro endothelial repair function in obstructive sleep apnea patients and impact of associated metabolic syndrome
Authors: Anne Briançon-Marjollet, Marion Henri, Emeline Lemarié, Jean-Louis Pépin, Renaud Tamisier, Patrick Lévy
Journal: European Respiratory Journal (2013)

The cardiovascular burden due to Obstructive Sleep Apnea (OSA) is a major health concern. Low grade vascular inflammation and endothelial dysfunction are two mechanisms involved into OSA related atherosclerosis. Interestingly, OSA patients exhibit an increase in plasma VEGF, but its function remains elusive. The aim of this study was to investigate serum factors from healthy controls (n=16), OSA patients free of any other disease (n=31), OSA patients with metabolic syndrome (MS)(n=21) and patients non-OSA with MS (n=13), affecting in vitro endothelial wound healing and monocyte migration.  Serum VEGF and usCRP levels were assessed and their specific function were tested with antibodies blocking VEGF or CRP (anti-CD32a) on endothelial cells (HMVEC) for wound healing assay and on human monocytic cell line for migration assay.  Along with the presence of OSA and/or MS, both VEGF and usCRP were significantly elevated in serum. Compared with controls, HMVEC wound healing was inhibited with OSA serum, and further with OSA+MS patient serum. It was also impaired when blocking VEGF in OSA serum and, by contrast, improved when blocking CRP. Monocyte migration was activated with OSA patient serum, and further enhanced by OSA+MS patient serum. Blocking CRP in serum inhibited this migration.  Thus, OSA patient serum alters in vitro endothelial cell repair function and activates monocyte migration; this is further aggravated with the presence of MS. These effects are partly driven by VEGF and CRP, suggesting an unfavorable balance between the pro healing (VEGF) and pro injury (CRP) factors that may promote vascular injury in OSA patients with and without MS.
Dermoscopy of black skin: A cross-sectional study of clinical and dermoscopic features of melanocytic lesions in individuals with type V/VI skin compared to those with type I/II skin
Authors: Bruna Tuma, Sergio Yamada, Álvaro Nagib Atallah, Fernanda Mendes Araujo, Sergio Henrique Hirata
Journal: Journal of the American Academy of Dermatology (2015)
YAP Promotes Malignant Progression of <i>Lkb1</i>-Deficient Lung Adenocarcinoma through Downstream Regulation of Survivin
Authors: Wenjing Zhang, Yijun Gao, Fuming Li, Xinyuan Tong, Yan Ren, Xiangkun Han, Shun Yao, Fei Long, Zhongzhou Yang, Hengyu Fan, Lei Zhang, Hongbin Ji
Journal: Cancer Research (2015)

Abstract The serine/threonine kinase LKB1 is a well-characterized tumor suppressor that governs diverse cellular processes, including growth, polarity, and metabolism. Somatic-inactivating mutations in LKB1 are observed in about 15% to 30% of non–small cell lung cancers (NSCLC). LKB1 inactivation confers lung adenocarcinomas (ADC) with malignant features that remain refractory to therapeutic intervention. YAP activation has been linked to LKB1 deficiency, but the role of YAP in lung ADC formation and progression is uncertain. In this study, we showed that ectopic expression of YAP in type II alveolar epithelial cells led to hyperplasia in mouse lungs. YAP overexpression in the KrasG12D lung cancer mouse model accelerated lung ADC progression. Conversely, YAP deletion dramatically delayed the progression of lung ADC in LKB1-deficient KrasG12D mice. Mechanistic studies identified the antiapoptotic oncoprotein survivin as the downstream mediator of YAP responsible for promoting malignant progression of LKB1-deficient lung ADC. Collectively, our findings identify YAP as an important contributor to lung cancer progression, rationalizing YAP inhibition in the context of LKB1 deficiency as a therapeutic strategy to treat lung ADC. Cancer Res; 75(21); 4450–7. ©2015 AACR.
Retraction statement: Steatohepatitis as impaired immune metabolism induced by liver‐resident regulatory T‐cell depletion
Authors: Shimazu Y, Hamaguchi M, Fukuda T, Yamaguchi K, Sumida Y, Tsuruyama T, Sparwasser T, Takaori-Kondo A, Fukui M, Itoh Y, Nakamura N
Journal: Hepatology (2015)

Yutaka Shimazu, Masahide Hamaguchi, Takuya Fukuda, Kanji Yamaguchi, Yoshio Sumida, Tatsuaki Tsuruyama, Tim Sparwasser, Akifumi Takaori‐Kondo, Michiaki Fukui, Yoshito Itoh, and Naoto Nakamura. Steatohepatitis as impaired immune metabolism induced by liver resident regulatory T‐cell depletion. H epatology 2015; doi: 10.1002/hep.27986. The above article, published online on July 14, 2015, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor in Chief, Michael H. Nathanson, the American Association for the Study of Liver Diseases, and Wiley Periodicals, Inc. The retraction has been agreed to due to insufficient permission by the authors' funding institution to submit and publish the manuscript. Reference Shimazu Y, Hamaguchi M, Fukuda T, Yamaguchi K, Sumida Y, Tsuruyama T, et al. Steatohepatitis as impaired immune metabolism induced by liver resident regulatory T‐cell depletion. Hepatology 2015; doi: 10.1002/hep.27986.Shimazu Y, Hamaguchi M, Fukuda T, Yamaguchi K, Sumida Y, Tsuruyama T, et al. Steatohepatitis as impaired immune metabolism induced by liver resident regulatory T‐cell depletion. H epatology 2015; doi: 10.1002/hep.27986.
Abstract 15962: VO2 Kinetics are Impaired in Patients With Heart Failure With Preserved Ejection Fraction (HFpEF)
Authors: Satyam Sarma, Paul S Bhella, Jeffrey L Hastings, Dean Palmer, Benjamin D Levine
Journal: Circulation (2014)

Background: VO2 kinetics, or mean response time (MRT), quantifies oxygen uptake at the onset of exercise reflecting the rapidity with which the cardiovascular system can match the metabolic demands of skeletal muscle. Slowed kinetics leads to myofibril oxygen deficit which must be buffered by increased glycolysis and depletion of high energy phosphate stores. To date no studies have assessed changes in VO2 kinetics in HFpEF but growing evidence suggests peripheral abnormalities in oxygen utilization play an important role in exertional intolerance. We hypothesized HFpEF patients would have prolonged MRT during exercise compared to healthy senior controls reflecting abnormalities in skeletal muscle oxygen utilization. Methods: Eight senior control and 13 carefully screened HFpEF subjects underwent cardiopulmonary exercise testing. AV nodal blocking agents were held 5 half-lives and subjects performed submaximal exercise at 30% of VO2max for 5 minutes. VO2 and cardiac output (Qc; acetylene rebreathe) were collected at rest and during exercise. MRT and O2 deficit were calculated from VO2 response curves plotted on a breath by breath basis. Results: HFpEF patients had lower peak VO2 compared to seniors (13.2 ± 3.1 vs 20.3 ± 3.5 ml/min/kg; p&lt;0.001). During fixed submaximal exercise, Qc, HR and VO2 were similar between groups. (Table) HFpEF patients had significantly prolonged MRT (69 v. 49s) compared to controls despite similar aerobic power and central cardiovascular and hemodynamic response. HFpEF patients also had a trend towards larger oxygen deficit (p=0.16) suggesting increased reliance on glycolytic metabolism during early exercise. Conclusions: HFpEF patients have slowed VO2 kinetics and an exaggerated O2 deficit during submaximal exercise. These findings establish abnormalities in muscle tissue oxygen utilization in HFpEF patients and suggest defects in oxygen metabolism are important contributors to exercise intolerance.
Histological typing of lung cancer in bioptically obtained specimens under the aspect of therapeutical approaches – A multi-center study
Authors: Annette Fisseler-Eckhoff, Rica Zinsky, Florian Laenger, Phillip Schnabel, Iver Petersen, Klaus Junker
Journal: European Respiratory Journal (2011)

The insufficiency of classifing lung cancer as SCLC or NSCLC clinical arose with the approval of the antifolate pemetrexed, which has a lower antitumorous effectivity in Squamous Cell Carcinoma. Often only biopsy specimens are available to exclude a squamous differentiation before chemotherapy decision.  The restrictive nature of subtyping lung cancer in biopsies demanded a skilled and experienced pathologist. This interlaboratory comparison should discover the accordance of subtyping of lung cancer biopsies evaluated in 5 different pathological institutes in germany. Is it possible to improve the accuracy histological typing by additional immunhistochemistry (IHC) panel?  60 biopsy specimens with Hematoxylin-eosin (HE) stain and immunhistological stained slides of at least Ck7, Ck5/6, p63, TTF1 were assembled and analysed from the pathologists. An estimation of predominantly-non-squamous yes/no and the histological subtype was done after examination the HE slide and again after the examination of the IHC. These two results were compared.  All 60 cases were analysed by all 5 participants. In average the agreement of predominantly-non-squamous with inspecting the HE slide was 50% and arose after IHC to 87%. The accordance of histological subtype arose from 58% after HE slide to 88% after IHC.  Histological subtyping of lung cancer biopsies can be done reliably with the help of an immunhistochemical panel of CK5/6, CK7, TTF1 and p63. Thus, we recommend the use of IHC to ensure diagnosis of lung cancer biopsies especially for patients coming into consideration for pemetrexed chemotherapy.
The Three Sisters: Transsexual Male Siblings
Authors: ROBERT F. SABALIS, ALLEN FRANCES, SUSAN N. APPENZELLER, WILLIE B. MOSELEY
Journal: American Journal of Psychiatry (1974)

This paper presents case material on three male siblings with a transsexual syndrome. It is probably the first such case recorded in the United States and may lead to the discovery of other such sibships, which could be of particular value in assessing the validity of some of the literature concerning the etiology of this disorder.
Effect of duration of treatment on treatment outcome and cost of treatment for Wilms' tumor: a report from the National Wilms' Tumor Study Group.
Authors: D M Green, N E Breslow, J B Beckwith, J Z Finklestein, P Grundy, P R Thomas, T Kim, S Shochat, G Haase, M Ritchey, P Kelalis, G J D'Angio
Journal: Journal of Clinical Oncology (1998)

PURPOSE National Wilms' Tumor Study (NWTS)-4 was designed to evaluate the efficacy, toxicity, and cost of the administration of different regimens for the treatment of Wilms' tumor (WT). PATIENTS AND METHODS Between August 6, 1986 and September 1, 1994, 905 previously untreated children aged younger than 16 years with stage II favorable histology (FH) WT (low-risk [LR]), stages III to IV FH WT, or stages I to IV clear-cell sarcoma of the kidney (high-risk[HR]) were randomized after the completion of 6 months of chemotherapy to discontinue (short) or continue for 9 additional months (long) treatment with chemotherapy regimens that included vincristine and either divided-dose (standard [STD]) courses (5 days) or single-dose (pulse-intensive [PI]) treatment with dactinomycin. HR patients also received either divided-dose (STD) courses (3 days) or single-dose (PI) treatment with doxorubicin. RESULTS The 4-year relapse-free survival (RFS) rates after the second randomization for LR patients were 83.7% for the 190 patients treated with short and 88.2% for the 187 patients treated with long chemotherapy (P = .11). The 4-year RFS rates after the second randomization for HR FH patients were 89.7% for the 256 patients treated with short and 88.8% for the 246 patients treated with long chemotherapy (P = .87). The charge for treatment with the short PI treatment regimens for all children with stages I through IV FH WT was approximately one half of that with the long STD treatment regimens. CONCLUSION The short administration schedule for the treatment of children with WT is no less effective than the long administration schedule and can be administered at a substantially lower total treatment cost.
Rapid quantification of bacteria associated to ventilator associated pneumonia in endotracheal aspirate specimens
Authors: Bruno François, Sandrine Prudent, Olivier Barraud, Morgane Lacroix, Marc Clavel, Marie-Astrid Jestin, Marc Rodrigue, Marie-Cécile Ploy, Alexandre Pachot, Javier Yugueros-Marcos, Virginie Moucadel
Journal: European Respiratory Journal (2014)

Ventilator-Associated Pneumonia (VAP) is one of the most serious infection in Intensive Care Unit. Today, its diagnosis relies mainly on conventional microbiological reports that are provided to the clinicians 24-72h after the sampling. Because an earlier diagnosis may reduce patient mortality and abusive use of antibiotics, we optimized a molecular biology-based method to quantify the DNA of bacteria frequently involved in VAP, directly from EndoTracheal Aspirates (ETA), in less than 3h30.  First, a Sample Processing Control is spiked into each 400 μL specimen. Second, the sample is submitted to a liquefaction process and an enzymatic lysis, and DNA is extracted using the easyMAG® system. Then, qPCR are run and DNA is quantified using standard curves.  Dynamic ranges for quantification were between ∼10^3 and ∼10^7 CFU/mL, depending on the bacterial target. The method was tested using ETA collected daily from mechanically ventilated patients (see patients 1 and 2, Figure 1) and we could follow the colonization with  S. aureus  over time. Indeed, the same trends were observed between the semi-quantitative culture and the ETA method.  Further assessment is now needed to evaluate the medical validity of this method for the early diagnosis of VAP, on larger populations.
Interstitial lung disease in the connective tisssue disease
Authors: Samira Aouadi, Asma Sebai, Houda Gharsalli, Houda Snene, Najla Ghrairi, Sonia Maalej, Leila El Gharbi
Journal: European Respiratory Journal (2014)

Introduction : Interstitial lung disease (ILD) is one of the most serious pulmonary complications associated with connective tissue diseases (CTD), resulting in significant morbidity and mortality. Usually, ILD occur in patients with diagnosed CTD. However, ILD can be the revealing manifestation of the disease.   Objective:  To describe clinical, radiological and laboratory finding in ILD associated with CTD.   Methods:  A retrospective study including all patients hospitalized between 2008 and 2013 for ILD associated with CTD was conducted in respiratory department D of A. Mami hospital.   Results:  twenty-five patients were includes (23 women, 2 men). Mean age was 55 years (29-78 years). CTD was previously diagnosed in 10 patients with a mean duration of 8 years. In 15 cases, the ILD was the revealing manifestation of the disease. Clinical extra pulmonary manifestations of CTD were found in 15 patients. The main CTD were Rheumatoid arthritis (n=10), poly-/dermatomyositis (n=6), Sjogren9s syndrome (n=4), systemic lupus erythematosus (n=3) and systemic sclerosis (n=2). Non-specific interstitial pneumonia was the most commonly observed pattern (n=13). The other patterns were usual interstitial pneumonia (n=9), organizing pneumonia (n=3). Serum antibodies were helpful in diagnosis of CTD in 23 cases. ILD was responsible for chronic respiratory failure in 4 cases and death in 2 cases.   Conclusion:  The possibility of CTD should be considered in patients with ILD. Careful examination and serum antibodies are very important for an early diagnosis of this association.
High-dose induction chemoradiotherapy followed by autologous bone marrow transplantation as consolidation therapy in rhabdomyosarcoma, extraosseous Ewing's sarcoma, and undifferentiated sarcoma.
Authors: F Boulad, N A Kernan, M P LaQuaglia, G Heller, K L Lindsley, N S Rosenfield, S J Abramson, W L Gerald, T N Small, A P Gillio, S C Gulati, R J O'Reilly, F Ghavimi
Journal: Journal of Clinical Oncology (1998)

To improve response and survival rates in patients with high-risk rhabdomyosarcoma (RMS), extraosseous Ewing's sarcoma, and undifferentiated sarcoma, we used a short course of induction with multi-agent chemotherapy, hyperfractionated radiotherapy, and surgery when possible. Consolidation was with intensive chemotherapy and autologous bone marrow transplantation (ABMT).Twenty-six patients (21 with RMS, three with undifferentiated sarcoma, and two with extraosseous Ewing's sarcoma) were entered onto the protocol between June 1990 and March 1994. Induction consisted of ifosfamide, etoposide, doxorubicin, dactinomycin, cyclophosphomide, and vincristine, and a split course of hyperfractionated radiotherapy. Patients who attained a complete response (CR) or good partial response (GPR) received consolidation with high-dose melphalan and etoposide followed by ABMT.Of 26 previously untreated patients 19 (73%) achieved a CR (n=13) or GPR (n=6) at the completion of induction and underwent ABMT. Two-year overall survival (OS) was 56% (95% confidence interval [CI], 36% to 76%) and progression-free survival (PFS) was 53% for the whole group (95% CI, 33% to 73%).Consolidation of response by myeloablative chemotherapy was well tolerated. Split-course hyperfractionated radiotherapy did not increase the rate of local control. The results of this short-course therapy were comparable to previous therapies of 1 to 2 years' duration. Induction and consolidation chemotherapy, as well as radiation dose, could be further intensified, since no death due to toxicity occurred among these patients.
Further Observations on the Inhibition of Tumor Growth by Corynebacterium parvum with Cyclophosphamide. IV. Effect of Rifampin on Tumor Growth Inhibition, Bone Marrow Macrophage Precursor Stimulation, and Macrophage Cytotoxicity2
Authors: Bernard Fisher, Herbert Rubin, Norman Wolmark
Journal: JNCI Journal of the National Cancer Institute (1976)

The cytotoxic macrophage was further characterized as an important effector cell in the inhibition of tumor growth. When we administered rlfampin (a semisynthetic antibiotic that interferes with macrophage function but not viability) with Corynebacterium parvum and/or cyclophosphamide to tumor-bearing C3HeB/FeJ female mice, the tumor growth-inhibitory effects of the C. parvum were reduced. Moreover, when bone marrow cells from those animals were cultured, we found a marked decrease in the cytotoxicity of macrophages comprising colonies arising from colony-forming cells (CFC) in the bone marrow. Such findings supported our contentions that 1) the cytotoxic property of macrophages originates in ancestral stem cells or CFC in bone marrow, and 2) receptor sites of the CFC (or stem cells) that respond to a stimulus for self-replication probably differ from sites that when activated produce progeny with cytotoxic properties. Although the administration of rifampin resulted in macrophages virtually devoid of cytotoxic properties, both relative and absolute numbers of CFC increased.