tbuckley/cabot-search huggingface dataset:
Insulin-like growth factor II-mediated proliferation of human neuroblastoma.
Authors: O M El-Badry, L J Helman, J Chatten, S M Steinberg, A E Evans, M A Israel
Journal: Journal of Clinical Investigation (1991)

Neuroblastoma is an embryonal tumor that typically arises in cells of the developing adrenal medulla. IGF-II mRNA is expressed at high levels in the adrenal cortex before birth but it is not detectable until after birth in the adrenal medulla. Neuroblastoma cell lines corresponding to early adrenal medullary precursors did not express IGF-II, although all three cell lines we tested were growth stimulated by IGF-II. Cell lines corresponding to more mature adrenal medullary cells expressed IGF-II, and one, SK-N-AS, grows by an IGF-II autocrine mechanism (J. Clin. Invest. 84:829-839) El-Badry, Romanus, Helman, Cooper, Rechler, and Israel. 1989. An examination of human neuroblastoma tumor tissues for IGF-II gene expression using in situ hybridization histochemistry revealed that IGF-II is expressed by tumor cells in only 5 of 21 neuroblastomas, but is detectable in cells of nonmalignant tissues including adrenal cortical cells, stromal fibroblasts, and eosinophils in all 21 tumors. These findings indicate that IGF-II may function as an autocrine growth factor for some neuroblastomas and as a paracrine growth factor for others. They suggest that the growth regulatory pathways utilized by neuroblastoma mimic those used in the precursor cell type from which individual tumors arise.
Impact of the Improved Patsari Biomass Stove on Urinary Polycyclic Aromatic Hydrocarbon Biomarkers and Carbon Monoxide Exposures in Rural Mexican Women
Authors: Horacio Riojas-Rodriguez, Astrid Schilmann, Adriana Teresa Marron-Mares, Omar Masera, Zheng Li, Lovisa Romanoff, Andreas Sjödin, Leonora Rojas-Bracho, Larry L. Needham, Isabelle Romieu
Journal: Environmental Health Perspectives (2011)

Cooking with biomass fuels on open fires results in exposure to health-damaging pollutants such as carbon monoxide (CO), polycyclic aromatic hydrocarbons (PAHs), and particulate matter.We compared CO exposures and urinary PAH biomarkers pre- and postintervention with an improved biomass stove, the Patsari stove.In a subsample of 63 women participating in a randomized controlled trial in central Mexico, we measured personal CO exposure for 8 hr during the day using continuous monitors and passive samplers. In addition, first-morning urine samples obtained the next day were analyzed for monohydroxylated PAH metabolites by gas chromatography/isotope dilution/high-resolution mass spectrometry. Exposure data were collected during the use of an open fire (preintervention) and after installation of the improved stove (postintervention) for 47 women, enabling paired comparisons.Median pre- and postintervention values were 4 and 1 ppm for continuous personal CO and 3 and 1 ppm for passive sampler CO, respectively. Postintervention measurements indicated an average reduction of 42% for hydroxylated metabolites of naphthalene, fluorene, phenanthrene, and pyrene on a whole-weight concentration basis (micrograms per liter of urine), and a 34% reduction on a creatinine-adjusted basis (micrograms per gram of creatinine). Pre- and postintervention geometric mean values for 1-hydroxypyrene were 3.2 and 2.0 μg/g creatinine, respectively.Use of the Patsari stove significantly reduced CO and PAH exposures in women. However, levels of many PAH biomarkers remained higher than those reported among smokers.
Failure of penicillin to alter acute rheumatic valvulitis
Authors: S. Vaisman
Journal: JAMA (1965)

A controlled study of the effects of penicillin on 165 patients with acute rheumatic fever has failed to demonstrate any alteration, attributable to the antibiotic, in valvular sequelae. The results suggest that the Streptococcus in the bacterial form does not play a continuing role in an acute episode of rheumatic fever once rheumatic symptoms have appeared.
Analysis of circulating immune complexes from patients with ankylosing spondylitis by gel electrophoresis and immunoblotting using antiserum against a psoriasis associated retrovirus-like particle.
Authors: E Rødahl, O.J Iversen
Journal: Annals of the Rheumatic Diseases (1986)

Circulating immune complexes (CIC) were isolated from patients with ankylosing spondylitis (AS) and healthy blood donors by isopycnic ultracentrifugation in sucrose gradients. The CIC were analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. The major components of the CIC were identified as albumin, immunoglobulins, and complement factors. A 70 kD component and several low molecular weight components (Mr 19 kD and 14 kD (doublet] were detectable only in CIC from patients with AS. An antiserum raised against the envelope glycoprotein, gp70, of a psoriasis associated retrovirus-like particle was applied to check for cross reacting activity. This antiserum reacted with both a 70 kD and a 40-45 kD component in CIC from three out of six patients but not with CIC from any of the blood donors.
DANGEROUS LIAISON: SUCCESSFUL PERCUTANEOUS EDGE–TO–EDGE MITRAL VALVE REPAIR IN PATIENTS WITH END–STAGE SYSTOLIC HEART FAILURE CAN CAUSE LEFT VENTRICULAR THROMBUS FORMATION
Authors: Martin Orban, Daniel Braun, Mathias Orban, Raffael Thaler, Hasema Lesevic, Julinda Mehilli, Steffen Massberg, Joerg Hausleiter
Journal: Journal of the American College of Cardiology (2013)
Waiting times for breast cancer test results have risen in past two years
Authors: C. White
Journal: BMJ (2003)

Patients with breast cancer report considerable improvements in care and treatment over the past five years, but waiting times for test results have crept up, a representative survey shows. And trusts are still not giving patients enough information about their disease.

The survey, commissioned by the charity Breakthrough Breast Cancer, details the responses of over 1200 women from 11 trusts across England about all stages of diagnosis and treatment of their disease.

The questions followed the themes identified in the NHS guidance Improving Outcomes in Breast …
Abstract 4592: Sox8 as a molecular marker of oligodendroglial tumors
Authors: Toshihiko Iuchi, Sana Yokoi, Miki Ohira, Hajime Kageyama, Makiko Itami, Yuzo Hasegawa, Koichiro Kawasaki, Tsukasa Sakaida, Akira Nakagawara
Journal: Cancer Research (2012)

Abstract Backgournd: The precise diagnosis of oligodendroglial tumors from astrocytic tumors is required because the sensitivity to treatments and outcome of patients are different between these two types of gliomas. However, morphological diagnosis of these tumors is not always easy and sometimes different among pathologists. The aim of this study is to clarify the clinical significance of Sox8 as a molecular marker of oligodendroglial tumors. Materials and Methods: The expression level of Sox8 was evaluated by real-time PCR in 74 gliomas (OII: 7, OIII: 15, AIII: 5, GBM: 47), and was compared with morphological diagnosis and other molecular markers as follows: 1p/19q co-deletion evaluated by array CGH, methylation of MGMT gene promoter by methylation-specific PCR, and IDH-1 mutation by immunohistochemistry. For the evaluation of diagnostic value of Sox8-expression, tumors were divided into two groups owing to the expression level of Sox8 (threshold: 2000), and the clinical outcome of patients were compared between these two groups. Furthermore, these diagnostic significances of Sox8 were compared with those of Olig-1 and Olig-2. Results: The expression level of Sox8 was significantly higher in oligodendroglial tumors (p&amp;lt;0.0001), 1p/19q co-deleted tumors (p&amp;lt;0.0001) and tumors with mutant IDH-1 protein (p&amp;lt;0.0001). The frequency of MGMT methylation was higher in tumors with high Sox8-expression, although statistical significance was not proven. In oligodendroglial tumors, the survival of patients with tumors exhibiting high Sox8-expression was significantly better than those with low SOX8-expression (hazard ratio: 6.2, p=0.031). High-expression of Olig-2 (hazard ratio: 4.5, p=0.026) and 1p/19q co-deletion (hazard ratio: 5.1, p=0.020) were also correlated with favorable outcome of patients, but no significant correlation between the expression of Olig-1 and patients’ outcome was observed. Conclusions: Sox8 was highly expressed in 1p/19q co-deleted oligodendroglial tumors. In oligodendroglial tumors, the expression of Sox8 was the significant prognostic factor of patients’ survival. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4592. doi:1538-7445.AM2012-4592
High molecular weight adiponectin inhibits proliferation of hepatic stellate cells via activation of adenosine monophosphate-activated protein kinase
Authors: Masayuki Adachi, David A. Brenner
Journal: Hepatology (2008)

Adiponectin is an adipocyte-derived, antidiabetic, antiatherogenic adipocytokine that is present in serum as 3 isoforms. Decreased plasma adiponectin levels are closely associated with the severity of nonalcoholic fatty liver diseases. This study was designed to elucidate a role of adiponectin and its mediator adenosine monophosphate-activated protein kinase (AMPK) on proliferation of activated hepatic stellate cells (HSCs), the key cells promoting fibrosis. Immortalized human HSC line hTERT and primary rat HSCs were stimulated with platelet-derived growth factor (PDGF) with or without pretreatment with AMPK activator 5-aminoimidazole-4-carboxamide-1-4-ribofuranoside (AICAR), metformin, or high molecular weight (HMW) adiponectin. HMW adiponectin dose-dependently suppressed PDGF-induced HSC proliferation. Adenoviral transduction with dominant-negative AMPK (DN-AMPK) abolished the suppressive effect of adiponectin in HSCs. AICAR, metformin, or transduction of constitutively active AMPK attenuated PDGF-induced [(3)H]thymidine incorporation, which was abolished by either a chemical AMPK inhibitor or transduction of DN-AMPK, consistent with an antiproliferative effect of AMPK. The suppressive effect of AMPK on HSC proliferation is mediated through multiple mechanisms, including (1) an inhibition of the AKT pathway, (2) inhibition of NADPH oxidase-dependent reactive oxygen species (ROS) production via induction of antioxidant enzymes, and (3) an increase in the expression of the cyclin-dependent kinase inhibitors p27(kip1) and p21(cip1).Adiponectin inhibits HSC proliferation via activation of AMPK. AMPK activation by AICAR or metformin inhibits HSC proliferation via suppression of ROS production and subsequent inhibition of AKT pathway. Thus, adiponectin and AMPK inhibit HSC proliferation and hepatic fibrosis via multiple molecular mechanisms.
Influence of ulcer healing agents on ulcer relapse after discontinuation of acute treatment: a pooled estimate of controlled clinical trials.
Authors: G Dobrilla, P Vallaperta, S Amplatz
Journal: Gut (1988)

Whether or not the incidence of ulcer relapse varies according to the drug used to produce initial healing is a controversial matter. We tackled this problem using data from 15 eligible trials from 25 published controlled trials in patients followed up for six to 12 months. Pooled estimates of differences in ulcer relapse incidence between patients initially healed with H2-antagonists and patients initially healed with non-H2-antagonist drugs were calculated. The overall incidence of relapse in patients healed with comparator drugs is 11 percentage units lower at six and 12 months, than that observed in H2-antagonist-healed patients. The confidence intervals are +/- 8% at six months and +/- 7% at 12 months. These data suggest the existence of a different effect on relapse incidence for the entire class of comparator drugs taken as a whole, compared with H2-antagonists. On considering the non-H2-antagonists singly, this conclusion holds good only in the case of tripotassium dicitrato bismuthate.
Randomized trial of ?-interferon or dexamethasone as maintenance treatment for multiple myeloma
Authors: Raymond Alexanian, Donna Weber, Meletios Dimopoulos, Kay Delasalle, Terry L. Smith
Journal: American Journal of Hematology (2000)

In order to assess the role of α-interferon or dexamethasone as maintenance therapy for multiple myeloma, 172 consecutive, previously untreated patients with disease of low or intermediate tumor mass received primary therapy with oral melphalan and intermittent, high-dose dexamethasone (MD), repeated monthly. Within 5 months, 84 responding patients were assigned at random to maintenance treatment with α-interferon (3 mU s.c. 3 × weekly) or dexamethasone (20 mg/m2 p.o. each morning for 4 days) repeated monthly until relapse. Upon relapse, MD was resumed for 2 cycles and second responses were maintained with 4-day courses of melphalan–dexamethasone until second relapse. Initial response was achieved in 88 patients (51%) after a median 0.7 month and no more than 3 courses of MD, a frequency of response similar to that observed previously with dexamethasone alone. There were identical median remissions of 10 months with interferon or dexamethasone, both maintenance regimens being associated with infrequent, mild, and reversible side effects. Significantly more patients responded again to resumption of MD after disease relapse to interferon (82%) than to dexamethasone (44%) (P = 0.001). The median remission from randomization to melphalan-resistant second relapse was 32 months for patients maintained initially on interferon compared to 19 months for those on dexamethasone (P = 0.01). These findings supported an advantage for interferon in remission maintenance by increasing the frequency of tumor recontrol with later treatment that included dexamethasone. Am. J. Hematol. 65:204–209, 2000. © 2000 Wiley-Liss, Inc.
Synergy between Celecoxib and Radiotherapy Results from Inhibition of Cyclooxygenase-2-Derived Prostaglandin E2, a Survival Factor for Tumor and Associated Vasculature
Authors: Thomas W. Davis, Janet M. O’Neal, Mark D. Pagel, Ben S. Zweifel, Pramod P. Mehta, Deborah M. Heuvelman, Jaime L. Masferrer
Journal: Cancer Research (2004)

Previous work has demonstrated that selective cyclooxygenase-2 (COX-2) inhibitors can act synergistically with radiotherapy to improve tumor debulking and control in preclinical models. The underlying mechanism of this remarkable activity has not yet been determined. Here, we report that radiation can elevate intratumoral levels of COX-2 protein and its products, particularly prostaglandin E(2) (PGE(2)). Furthermore, inhibition of COX-2 activity or neutralization of PGE(2) activity enhances radiotherapy even in tumors where COX-2 expression is restricted to the tumor neovasculature. Direct assessment of vascular function by direct contrast enhancement-magnetic resonance imaging showed that the combination of radiation and celecoxib lead to enhanced vascular permeability. These observations suggest that an important mechanism of celecoxib-induced radiosensitization involves inhibition of COX-2-derived PGE(2), thus removing a survival factor for the tumor and its vasculature.
Trendelenburg's Operation for Removal of a Pulmonary Embolus
Authors: N. C. Lake
Journal: BMJ (1927)

8RTApars intermedia.The pars glandularis is intensely con- gested; otherwise there is no evidence of pathological c}ange.The case is of interest as exhibiting the presence of ocular symptoms in the absence of glandular or neighbour- hiood phenomena.This incongruity fortunately delayed operative measures, and so prevented what might otherwise have proved catastrophic surgical interventioni.FAMILIAL PELLAGRA IN IRELAND.
We Physicians Are Fiduciary Failures
Authors: George B. Markle
Journal: JAMA (1978)

IT IS difficult for most members of the medical profession to think of themselves in the role of a fiduciary, especially since many of us not versed in financial jargon do not even know what a fiduciary is. In essence, a fiduciary is a person (or an institution) who holds something of value for another in trust.  When one looks at the costs of medical care today, it should become apparent that we are responsible for more than just the physical well-being of the patient; we are in a position to bankrupt him or the society that pays for his care. Every time we order a test or a roentgenogram, send a patient for a consultation, prescribe a medicine or a therapeutic procedure, or admit a patient to the hospital, we are investing his money on his behalf, supposedly for his own health. It is the same as though a
Histamine and interstitial Pulmonary Edema in the Dog
Authors: G. G. Pietra, J. P. Szidon, M. M. Leventhal, A. P. Fishman
Journal: Circulation Research (1971)

Histamine, administered to dogs by various routes, produced peribronchial interstitial edema. Using colloidal carbon as an electron-dense tracer, it was shown that bronchial venules had become leaky at the same time that the minute blood vessels of the pulmonary circulation remained unaffected by the histamine. The effect of histamine was rapid and brief in duration: wide interendothelial gaps appeared in the walls of bronchial venules through which blood and tracer escaped into the interstitium. This action of histamine seemed to be related to the presence in the bronchial venular endothelium of abundant cytoplasmic fibrils that presumably have contractile capacity. Water content of the lungs was consistent with morphologic evidence that histamine promoted the accumulation of fluid in the lungs. The same pattern of response was observed after bradykinin or compound 48/80, a mast cell degranulator. In contrast to these three agents, serotonin did not affect bronchial venular permeability to colloidal carbon. Consideration of these observations in the light of the large extent of the bronchial venular plexus, raises the possibility that the bronchial venular system may play an important reabsorptive role under normal circumstances and that it may also be involved in the genesis of certain types of interstitial pulmonary edema.
42. Uniform Scale-Independent Gene Transfer to Striated Muscle after Transvenular Extravasation of Vector
Authors: Kapil Gopal, Leonard T. Su, Zhonglin Wang, Xiaoqing Yin, Anthony Nelson, Benjamin W. Kozyak, James M. Burkman, Marilyn A. Mitchell, David W. Low, Charles R. Bridges, Hansell H. Stedman
Journal: Molecular Therapy (2005)

Top of pageAbstract
The muscular dystrophies exemplify a class of systemic disorders for which widespread protein replacement in situ is essential for full complementation of the underlying genetic disorder. As a direct approach to this clinical challenge, somatic gene transfer will require efficient, scale-independent transport of DNA-containing macromolecular complexes too large to cross the continuous endothelia under physiological conditions. Previous studies in large animal models have revealed a trade-off between the efficiency of gene transfer and the inherent safety of the required surgical and pharmacological interventions. We tested the hypothesis that rapid, mechanical distention of the post-capillary venular endothelium by afferent infusion from a distal site would safely facilitate macromolecular transport from the vascular space to the striated muscle interstitium. We show that pressurized infusion through a large-bore catheters in either peripheral, superficial veins or the coronary sinus results in uniform, scale-and vector-independent transduction of myofibers in anatomic domains isolated from the remainder of the circulation. This approach is rapid, minimally invasive as applied to the isolated limb, and avoids pharmacological interference with cardiovascular homeostasis. We provide the first demonstration of uniform gene transfer to virtually 100% of the muscle fibers of an entire extremity in the dog, providing a firm foundation for studies of efficacy in canine models for human diseases. Additional data from a combination of angiographic, tracer dye, and marker gene studies suggests that this approach can be modified to meet the requirements for cardiac-specific or systemic gene delivery as appropriate in a variety of inherited and acquired diseases including hemophilia, muscular dystrophy, and cardiomyopathy.

Figure 1 |[ndash]| |[beta]|-galactosidase levels of rat limb, rat cardiac and dog limb muscles after no treatment, vector delivery without afferent transvenular retrograde extravasation (ATVRX) and vector delivery with ATVRX.

Figure 2 |[ndash]| LacZ expression after rat quadriceps (left), rat heart (middle), and dog vastus medialis (right) stained with x-galactosidase.
Allergy to feathers
Authors: K. Kilpiö, S. Mäkinen‐Kiljunen, T. Haahtela, M. Hannuksela
Journal: Allergy (1998)

Skin prick test reactivity to commercial and self-made feather-allergen extracts was examined in 269 consecutive adult patients with suspected allergic cutaneous or respiratory symptoms who had been referred to a university clinic. Some 177 subjects reacted to any inhalant allergen. Twenty-four (9% of the whole group and 14% of those positive to any inhalant allergen) reacted to commercial feather extracts from ALK (Hørsholm, Denmark), and 51 to any of the seven feather extracts used. Feather-mix RAST (Pharmacia, Sweden) was positive in three cases only. Skin prick test or CAP-RAST or both to house-dust mite were positive in 16 of those 24 subjects positive to the commercial feather extracts, but in only 23 of the 150 other atopic subjects (P < 0.001). A nasal challenge with a feather extract was made in 20 cases, always with negative result. In immunospot studies, concomitant allergy to feather-allergen extracts and house-dust mite could be demonstrated. Mite allergens in feather extracts were verified in RAST-inhibition studies. A clinically significant feather allergy was found in one patient only. The results suggest that true feather allergy is very rare, and most of the positive reactions seen in skin prick tests to feather extracts are probably caused by mite allergens present in feathers.
Effects of a predominantly hydroxyethyl starch (HES)-based and a predominantly non HES-based fluid therapy on renal function in surgical ICU patients
Authors: Franziska Schabinski, Janaina Oishi, Fabio Tuche, Alain Luy, Yasser Sakr, Donald Bredle, Christiane Hartog, Konrad Reinhart
Journal: Intensive Care Medicine (2009)
Regulation of the Immune Response — Role of the Macrophage
Authors: Alan S. Rosenthal
Journal: New England Journal of Medicine (1980)

MACROPHAGES facilitate a variety of thymus-dependent immunologic phenomena in human beings and laboratory animals; thus, these cells are essential for the development of cellular and humoral immunocompetence.1 ,1a Their role in T-cell and B-cell function is shown schematically in Figure 1. Macrophages serve at least four distinct but interlocking functions in host defense. First of all, the induction of T-lymphocyte proliferation requires the physical association of the T cells with macrophages bearing antigen.1b Secondly, the macrophage is a principal site of control by the immune-response gene.2 Thirdly, macrophages have several plasma-membrane receptors, such as those for the Fc portion of IgG, that . . .