tbuckley/cabot-search huggingface dataset:
Induction of Delayed Hypersensitivity to Human Tumor Cells With a Human Monoclonal Anti-idiotypic Antibody
Authors: E. B. Austin, R. A. Robins, R. W. Baldwin, L. G. Durrant
Journal: JNCI Journal of the National Cancer Institute (1991)

There is considerable interest in the development of anti-idiotypic antibodies as vaccines in a number of diseases, including cancer. We have developed a human anti-idiotypic monoclonal antibody (105AD7) which binds at or very near to the binding site of mouse antitumor monoclonal antibody 791T/36. The 791T/36 antibody binds to a tumor-associated antigen (gp72) expressed on a number of human tumors, including colorectal and ovarian carcinomas and osteogenic sarcoma. This study shows that, in rats and mice, 105AD7 induces delayed-type hypersensitivity to human tumor cells bearing the gp72 antigen. Local transfer of delayed hypersensitivity was also demonstrated using lymphocytes from mice primed with 105AD7. These findings show that the human monoclonal anti-idiotypic antibody 105AD7 is likely to induce cellular immune responses to tumors in cancer patients.
Role of the Allergist in Diagnosis and Management of Patients With Uveitis
Authors: Thomas E. Van Metre
Journal: JAMA (1966)

The allergist confronted by a patient with uveitis must be prepared to use many different diagnostic approaches and treatments which will be determined by the characteristics of the patient's disease. Close teamwork between allergist and ophthalmologist is essential. The ophthalmologist defines the morphology and course of the ocular lesion and the possible causes indicated thereby. The allergist determines which of these possible causes is present. Both must supervise treatment: the ophthalmologist concerned with the response of the eye; the allergist, with the response of the body, particularly where therapy with systemic effect must be used, such as vaccines, corticosteroids, and antimicrobial agents.
Dopamine attenuates the contractile response to angiotensin II in isolated rat glomeruli and cultured mesangial cells.
Authors: R Barnett, P C Singhal, L A Scharschmidt, D Schlondorff
Journal: Circulation Research (1986)

Recent evidence suggests that dopamine may alter kidney function by actions not only in the renal vasculature but also at the glomerular-mesangial level. We studied this phenomenon by examining the ability of dopamine to antagonize the contractile properties of angiotensin II in isolated rat glomeruli and cultured mesangial cells. In isolated rat glomeruli angiotensin II caused a decrease in the planar surface area, indicating glomerular contraction, an effect that was abolished by coincubation with dopamine. Angiotensin II also mediated shape changes in cultured mesangial cells, which resulted in a decline in their planar areas. Simultaneous addition of dopamine prevented these decreases in cell size. In mesangial cells grown on a flexible silicone rubber support, angiotensin II addition enhanced wrinkling of the mobile surface. This indicated that the angiotensin-II-induced decrease in cell size observed in cells grown on conventional substrata represented contraction. Conversely, dopamine caused a rapid reduction in wrinkling of the surfaces from control cells as well as those previously treated with angiotensin II, actions consistent with cell relaxation. The prostaglandin inhibitor indomethacin did not alter the ability of dopamine to attenuate angiotensin-II-associated reductions in mesangial cell surface area. Direct determination of mesangial cell prostaglandin-E2 production showed that dopamine did not change either basal synthesis or angiotensin-II-stimulated synthesis of prostaglandin. The results demonstrate that dopamine antagonizes the constrictor effect of angiotensin II at the glomerular-mesangial level. This action of dopamine is prostaglandin independent. These findings support a role for dopamine in the regulation of glomerular filtration and may provide a rationale for its use during states of renal vasoconstriction.
Increased myocardial collagen and ventricular diastolic dysfunction in relaxin deficient mice: a gender-specific phenotype
Authors: X Du
Journal: Cardiovascular Research (2003)

Objective: To investigate cardiac phenotypes in mice deficient in the peptide hormone relaxin by gene targeting. Methods: Echocardiography and cardiac catheterization were performed on male and female relaxin deficient (Rlx−/−) mice as well as heterozygous (Rlx+/−) and wildtype (Rlx+/+) littermates aged between 8 and 24 months. Collagen expression and content in the heart were analysed by real-time PCR, hydroxyproline assay and histology. Results: Heart rate, blood pressures, left ventricular (LV) dimensions, fractional shortening and maximal and minimal dP/dt did not differ significantly between the three genotypes of either gender at any age. However, 8–10-month-old Rlx−/− males exhibited a greater transmitral flow velocity (A-wave) at the late LV diastolic phase. Male Rlx−/− mice aged between 12 and 24 months had significantly higher LV end-diastolic pressures, a 30% increase in atrial weight and 10–30% increases in lung and liver weights. Male mice also showed an age-dependent increase (P<0.01) in LV collagen content that was more pronounced in Rlx−/− than control littermates (P<0.01). Procollagen type-1 expression was also significantly higher in the LV of Rlx−/− males compared with either Rlx+/− or Rlx+/+ males at 6, 9 and 12 months of age. Age-matched female Rlx−/− mice did not display any of these cardiac phenotypes seen in Rlx−/− males. Conclusions: Male Rlx−/− mice had impeded LV diastolic filling and increased atrial weights, most likely due to an increase in ventricular collagen content and chamber stiffness. These phenotypes in the Rlx−/− males were not observed in Rlx−/− females, indicating the importance of other gender-related factors in cardiovascular function.
Lifestyle Intervention Development Study to Improve Physical Function in Older Adults With Cancer: Outcomes From Project LEAD
Authors: Wendy Demark-Wahnefried, Elizabeth C. Clipp, Miriam C. Morey, Carl F. Pieper, Richard Sloane, Denise Clutter Snyder, Harvey J. Cohen
Journal: Journal of Clinical Oncology (2006)

Declines in physical functioning (PF) among elderly cancer patients threaten quality of life and the ability to maintain independence. Adherence to healthy lifestyle behaviors may prevent functional decline.Project Leading the Way in Exercise and Diet (LEAD), an intervention development study of the Pepper Older Americans Independence Center, aimed to determine whether breast and prostate cancer survivors (age 65+ years) assigned to a 6-month home-based diet and exercise intervention experienced improvements in PF when compared with an attention control arm receiving general health information. An accrual target was set at 420, and PF (Short Form-36 subscale), physical activity (Community Healthy Activities Models Program for Seniors), and diet quality (index from 3-day recalls) were assessed at baseline and at 6 and 12 months (6 months after intervention).This developmental project did not achieve its accrual target (N = 182); however, PF change scores were in the direction and of the magnitude projected. Baseline to 6-month change scores in the intervention versus the control arms were as follows: PF, +3.1 v -0.5 (P = .23); physical activity energy expenditure, +111 kcal/wk v -400 kcal/wk (P = .13); and diet quality index, +2.2 v -2.9 (P = .003), respectively. Differences between arms diminished during the postintervention period.These findings suggest that home-based diet and exercise interventions hold promise in improving lifestyle behaviors among older cancer survivors, changes that trend toward improved PF. Future studies should incorporate larger sample sizes and interventions that sustain long-term effects and also take into account secular trends; these efforts will require adequate planning and resources to overcome the numerous barriers to intervening in this difficult to reach yet vulnerable population.
Detecting PE in COPD
Authors: Vinod Aiyappan
Journal: Thorax (2007)

▴ Monreal M, Munoz-Torrero JF, Naraine VS, et al . Pulmonary embolism in patients with chronic obstructive pulmonary disease or congestive heart failure. Am J Med2006;119:851–8.

[OpenUrl][1][CrossRef][2][PubMed][3][Web of Science][4]



Pulmonary embolism (PE) is a difficult diagnosis to make or exclude and there have been various pretest probability scoring systems developed to aid the clinician in this area. However, these scoring systems do not take into account underlying cardiopulmonary abnormalities. This interesting study by Monreal et al looked at …

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Emergency oxygen use
Authors: R. O'Driscoll
Journal: BMJ (2012)

<h3>Abstract</h3> Airway epithelial damage is a common feature in respiratory diseases such as COPD and has been suggested to drive inflammation and progression of disease. These features manifest as remodeling and destruction of lung epithelial characteristics including loss of small airways which contributes to chronic airway inflammation. Histone deacetylase 6 (HDAC6) has been shown to play a role in epithelial function and dysregulation, such as in cilia disassembly, epithelial to mesenchymal transition (EMT) and oxidative stress responses, and has been implicated in several diseases. We thus used ACY-1083, an inhibitor with high selectivity for HDAC6, and characterized its effects on epithelial function including epithelial disruption, cytokine production, remodeling, mucociliary clearance and cell characteristics. Primary lung epithelial air-liquid interface cultures from COPD patients were used and the impacts of TNF, TGF-β, cigarette smoke and bacterial challenges on epithelial function in the presence and absence of ACY-1083 were tested. Each challenge increased the permeability of the epithelial barrier whilst ACY-1083 blocked this effect and even decreased permeability in the absence of challenge. TNF was also shown to increase production of cytokines and mucins, with ACY-1083 reducing the effect. We observed that COPD-relevant stimulations created damage to the epithelium as seen on immunohistochemistry sections and that treatment with ACY-1083 maintained an intact cell layer and preserved mucociliary function. Interestingly, there was no direct effect on ciliary beat frequency or tight junction proteins indicating other mechanisms for the protected epithelium. In summary, ACY-1083 shows protection of the respiratory epithelium during COPD-relevant challenges which indicates a future potential to restore epithelial structure and function to halt disease progression in clinical practice.
Prenatal exclusion of harlequin ichthyosis; potential pitfalls in the timing of the fetal skin biopsy
Authors: A. Shimizu, M. Akiyama, A. Ishiko, T. Yoshiike, K. Suzumori, H. Shimizu
Journal: British Journal of Dermatology (2005)

Background Harlequin ichthyosis (HI) is a severe and usually fatal congenital skin disorder with autosomal recessive inheritance. Several cases of HI prenatal diagnosis have been performed using fetal skin biopsy, mainly at around 23 weeks estimated gestational age (EGA), and reported in the literature. However, prenatal testing must be done earlier than 21 weeks EGA in several countries including Japan where the present HI families live, because termination is legally allowed only until 22 weeks EGA.
Retrospective Assessment of Hypercoagulability in Breast Cancer Prevention Trial
Authors: Neil Abramson, Richard H. Aster
Journal: Journal of Clinical Oncology (2002)

Article Tools SPECIAL DEPARTMENTS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2002.99.155 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 12351619 Retrospective Assessment of Hypercoagulability in Breast Cancer Prevention Trial Neil AbramsonxNeil AbramsonSearch for articles by this author , Richard H. AsterxRichard H. AsterSearch for articles by this author Show More Baptist Cancer Institute, Jacksonville, FLThe Blood Center, Milwaukee, WI https://doi.org/10.1200/JCO.2002.99.155 First Page Full Text PDF Figures and Tables © 2002 by American Society of Clinical Oncology
Signal Transducers and Activators of Transcription 3 Pathway Activation in Drug-Resistant Ovarian Cancer
Authors: Zhenfeng Duan, Rosemary Foster, Debra A. Bell, Jennifer Mahoney, Kathryn Wolak, Ami Vaidya, Constanze Hampel, Hang Lee, Michael V. Seiden
Journal: Clinical Cancer Research (2006)

Abstract Purpose: One of the major obstacles in the treatment of ovarian cancer is the development of multidrug resistance. Recent evidence shows that high-grade ovarian cancer often shows activation of the signal transducers and activators of transcription 3 (Stat3) pathway with subsequent transcription of genes that support tumor growth and survival. Less studied is the role of the Stat3 pathway in acquired drug resistance. There is no information on Stat3 expression in chemotherapy naïve ovarian cancer as compared with tumors collected later in the natural history of the disease. To further clarify the significance of Stat3 activation in ovarian cancer, here we investigated the Stat3 expression and activation in ovarian cancer and ovarian cancer multidrug resistance cell lines. Experimental Design: Western blotting, electrophoretic mobility shift assay, luciferase assays, ELISA assay, and real-time reverse transcription-PCR determined interleukin-6 and Stat3 pathway expression and activation in cell lines. Stat3 expression in ovarian cancer tissue microarray was evaluated by immunohistochemistry. Results: Activated (phosphorylated) Stat3 is overexpressed in most paclitaxel-resistant ovarian cancer cells. Inhibition of Stat3 activation results in significant decreases in paclitaxel resistance and enhanced apoptosis. Drug-resistant recurrent tumors have significantly greater phosphorylated Stat3 (pStat3) expression as compared with matched primary tumors. Tumors with associated inflammatory cell infiltrates also have a higher proportion of cells staining intensely for nuclear phosphorylated Stat3 as compared with tumors without inflammatory infiltrates, consistent with paracrine activation of the Stat3 pathway by immune-mediated cytokines. Conclusions: These data support the hypothesis that interruption of Stat3 signaling could reverse resistance to paclitaxel and perhaps other chemotherapy agents in human cancer.
Reduced-intensity conditioning allogeneic stem cell transplantation for relapsed/refractory mantle cell lymphoma: a multicenter experience
Authors: S. Le Gouill, N. Kröger, N. Dhedin, A. Nagler, K. Bouabdallah, I. Yakoub-Agha, T. Kanouni, C.E. Bulabois, O. Tournilhac, A. Buzyn, B. Rio, M.P. Moles, A. Shimoni, U. Bacher, S. Ocheni, N. Milpied, J.L. Harousseau, P. Moreau, C. Leux, M. Mohty
Journal: Annals of Oncology (2012)
Adenovirus-Mediated Transfer of Human Placental Ectonucleoside Triphosphate Diphosphohydrolase to Vascular Smooth Muscle Cells Suppresses Platelet Aggregation In Vitro and Arterial Thrombus Formation In Vivo
Authors: Eiji Furukoji, Masanori Matsumoto, Atsushi Yamashita, Hideo Yagi, Yoshihiko Sakurai, Kousuke Marutsuka, Kinta Hatakeyama, Kazuhiro Morishita, Yoshihiro Fujimura, Shozo Tamura, Yujiro Asada
Journal: Circulation (2005)

Background— Platelet-rich thrombus formation is a critical event in the onset of cardiovascular disease. Because ADP plays a significant role in platelet aggregation, its metabolism is important in the regulation of platelet activation and recruitment. Ectonucleoside triphosphate diphosphohydrolase (E-NTPDase) is a key enzyme involved in vascular ADP metabolism. We recently isolated 2 isoforms of E-NTPDase from the human placenta. The present study examined whether these isoforms suppress platelet aggregation and thrombus formation after adenovirus-mediated gene transfer to vascular smooth muscle cells (SMCs). Methods and Results— We constructed adenovirus vectors expressing human placental E-NTPDase isoforms I (AdPlac I) and II (AdPlac II) or bacterial β-galactosidase (AdLacZ). Vascular SMCs infected with AdPlac I expressed significant NTPDase activity and inhibited the platelet aggregation induced by ADP and collagen in vitro. In contrast, SMCs infected with AdPlac II and AdLacZ did not exert antiplatelet effects. To investigate the antithrombotic and antiproliferative effects of placental E-NTPDase isoform I in vivo, we generated thrombosis in rat carotid arteries by systemically administered rose Bengal and transluminal green light 5 days after gene transfer and examined neointimal growth 3 weeks after thrombus formation. Blood flow in AdLacZ-infected arteries rapidly deteriorated and vanished within 96±18 seconds of occlusive thrombus formation. In contrast, blood flow in AdPlac I–infected arteries was preserved for at least 10 minutes during irradiation. In addition, thrombus formation and subsequent neointimal growth were obviously suppressed. Conclusions— The local expression of placental E-NTPDase in injured arteries might prevent arterial thrombosis and subsequent neointimal growth.
The gold standard: not a golden standard
Authors: Jurgen A H R Claassen
Journal: BMJ (2005)

potential for confounding.Could the negative finding from this analysis be due to confounding?If so, some factor(s) would have to be negatively associated with Crohn's disease, be introduced over the same three year period, and be targeted at the same population of infants as MMR vaccine to mask a true association.This seems highly unlikely.A smaller ecological study 2 and two case-control studies 3 w3 also found no increased risk of Crohn's disease associated with MMR vaccine.Initially, measles vaccine was reported to be associated with higher rates of Crohn's disease, 4 but this was not confirmed by subsequent studies. 3 5Natural infections with measles and mumps within one year were also associated with an increased risk of Crohn's disease.w4 Although that finding has yet to be confirmed, it raised the possibility that infections with multiple viruses in MMR vaccine might increase the risk of Crohn's disease.My study provides strong evidence against that hypothesis and adds to the evidence that MMR vaccine is no less safe in this respect than the single measles vaccine.
Etanercept maintains the clinical benefit achieved by infliximab in patients with rheumatoid arthritis who discontinued infliximab because of side effects
Authors: F. Iannone, F. Trotta, C. Monteccuco, R. Giacomelli, M. Galeazzi, M. Matucci-Cerinic, C. Ferri, M. Cutolo, L. Maria Bambara, G. Triolo, G. Ferraccioli, G. Valentini, G. Lapadula
Journal: Annals of the Rheumatic Diseases (2006)

To evaluate the efficacy of switching to etanercept treatment in patients with rheumatoid arthritis who already responded to infliximab, but presented side effects.Charts of 553 patients with rheumatoid arthritis were retrospectively reviewed to select patients who responded to the treatment with infliximab and switched to etanercept because of occurrence of adverse effects. Clinical data were gathered during 24 weeks of etanercept treatment and for the same period of infliximab treatment before infliximab was stopped. Disease Activity Score computed on 44 joints (DAS-44), erythrocyte sedimentation rate (ESR) 1st hour, Visual Analogue Scale (VAS) of pain, Health Assessment Questionnaire (HAQ), and C reactive protein (CRP) were assessed every 8 weeks.37 patients were analysed. Adverse events to infliximab were mostly infusion reactions. No statistically significant difference between infliximab, before withdrawal, and etanercept, after 24 weeks, was detected in terms of DAS-44 (2.7 and 1.9, respectively), HAQ (0.75 and 0.75, respectively), ESR (21 and 14, respectively) and CRP (0.5 and 0.3, respectively). VAS pain decreased significantly after switching to etanercept treatment (40 and 24, respectively; p<0.05).Our study shows that etanercept maintains the clinical benefit achieved by infliximab, and suggests that a second tumour necrosis factor (TNF) alpha inhibitor can be the favourable treatment for rheumatoid arthritis when the first TNFalpha blocker has been withdrawn because of adverse events.
Hypothermia Induced in a Myxoedematous Patient by Imipramine Hydrochloride
Authors: M. D. McGrath, R. G. Paley
Journal: BMJ (1960)

Hypothermia Induced in a MyxoedematousPatient by Imipramine HydrochlorideThe " cooling " effect of the phenothiazines, particularly chlorpromazine, is well known (Courvoisier et al., 1953).Mitchell et al. (1959) have shown that chlorpromazine can precipitate a hypothermic myxoedema coma in a hypothyroid patient.A similar pharmacological action would not be surprising from chlorpromazine and imipramine hydrochloride (" tofranil ") owing to the close structural similarity of these two agents:
Targeting CXCR7/ACKR3 as a therapeutic strategy to promote remyelination in the adult central nervous system
Authors: Jessica L. Williams, Jigisha R. Patel, Brian P. Daniels, Robyn S. Klein
Journal: The Journal of Experimental Medicine (2014)

Current treatment modalities for the neurodegenerative disease multiple sclerosis (MS) use disease-modifying immunosuppressive compounds but do not promote repair. Although several potential targets that may induce myelin production have been identified, there has yet to be an approved therapy that promotes remyelination in the damaged central nervous system (CNS). Remyelination of damaged axons requires the generation of new oligodendrocytes from oligodendrocyte progenitor cells (OPCs). Although OPCs are detected in MS lesions, repair of myelin is limited, contributing to progressive clinical deterioration. In the CNS, the chemokine CXCL12 promotes remyelination via CXCR4 activation on OPCs, resulting in their differentiation into myelinating oligodendrocytes. Although the CXCL12 scavenging receptor CXCR7/ACKR3 (CXCR7) is also expressed by OPCs, its role in myelin repair in the adult CNS is unknown. We show that during cuprizone-induced demyelination, in vivo CXCR7 antagonism augmented OPC proliferation, leading to increased numbers of mature oligodendrocytes within demyelinated lesions. CXCR7-mediated effects on remyelination required CXCR4 activation, as assessed via both phospho-S339-CXCR4-specific antibodies and administration of CXCR4 antagonists. These findings identify a role for CXCR7 in OPC maturation during remyelination and are the first to use a small molecule to therapeutically enhance myelin repair in the demyelinated adult CNS.