tbuckley/cabot-search huggingface dataset:
NI-44 * LIPOSOMAL NANOPARTICLES FOR TARGETING AND IMAGING OF PEDIATRIC BRAIN TUMORS
Authors: M. Kambhampati, S. Yadavilli, K. M. McNeeley, S. B. Pai, Q. Yu, R. Bellamkonda, R. Fernandes, R. J. Packer, J. Nazarian
Journal: Neuro-Oncology (2014)

BACKGROUND: This study reports the targeting and real-time optical imaging of brainstem tumors using liposomal nanocarriers. Patients with infiltrating brainstem gliomas (BSG) known as diffuse intrinsic pontine gliomas (DIPGs) have one of the poorest survival rates. Blood brain barrier (BBB) is the main obstacle in the delivery of drugs and contrast agents to DIPGs. OBJECTIVE: Here, we demonstrate the specific delivery of liposomal nanoparticles containing Evans blue (nano-EB) to tumor in a murine model of BSG. METHODS/DESIGN: Mice with brainstem tumors were tail vein injected with nano-EB and in vivo tumor enhancement was monitored by optical fluorescence imaging. RESULTS/DISCUSSION: Necropsy analysis conducted 24 hr post injection showed site-specific delivery of nano-EB to the tumor but not adjacent normal tissue. Immunohistochemical assays confirmed high grade tumor at the site of nano-EB accumulation. These findings demonstrate the feasibility of nano-EB for drug delivery and real-time, sensitive optical imaging of BSGs in vivo. The study shows the specific accumulation of liposomal nano-EB nanocarriers in brainstem tumors in our murine model of brainstem glioma. Liposomes are an ideal drug delivery vehicle able to cross the BBB . Specific accumulation of nano-EB in tumor cells is explained by the enhanced permeability and retention (EPR) property of cancer cells which is believed to be due to the abnormal neovasculature with poorly-aligned defective endothelial cells and structure. This pilot study shows the efficacy of liposomes for targeted delivery and possibility of using nano-EB for in vivo imaging of tumors in a murine model of brain tumors.
1070 THE VALUE OF ARFI ELASTOGRAPHY FOR FIBROSIS EVALUATION IN PATIENTS WITH CHRONIC HEPATITIS C IN COMPARISON WITH LIVER BIOPSY-AN INTERNATIONAL MULTICENTER STUDY
Authors: I. Sporea, S. Bota, R. Sirli, H. Tanaka, H. Iijima, R. Badea, M. Lupsor, C. Fierbinteanu-Braticevici, A. Petrisor, H. Saito, H. Ebinuma, M. Friedrich-Rust, C. Sarrazin, H. Takahashi, N. Ono, F. Piscaglia, A. Borghi, M. D'Onofrio, A. Gallotti, M. Peck-Radosavljevic, A. Ferlitsch, A. Popescu, M. Danila
Journal: Journal of Hepatology (2012)
Effect of aldosterone on the coupling between H+ transport and glucose oxidation.
Authors: Q Al-Awqati
Journal: Journal of Clinical Investigation (1977)

The mode of action of aldosterone on the energetics of H+ transport in the turtle bladder was examined with the rate of glucose oxidation as an index of the metabolic activity of the epithelium (we show that H+ transport is not coupled to fatty acid oxidation). Within 6 h of addition of aldosterone H+, transport increased; so did glucose oxidation. The amount of H+ transport per mole of 14CO2 produced from glucose oxidation was 15.6 eq-mol-1 in the control hemi-bladder, while in the aldosterone-treated bladder it was 13.6, delta = 2.0+/-4.0 (n = 6). However, in bladders exposed to aldosterone for 20 h, the relation of transport to glucose oxidation was significantly altered: control 10.8, aldosterone 16.4, delta = 4.5+/-2.5, P less than 0.02, n = 7. The slope of H+ transport on the applied electrochemical gradient was steeper during both short- and long-term incubations. However, the maximum gradient necessary to nullify the net rate of secretion was unaltered in both experiments. Evidence is presented that aldosterone does not alter the passive backflux into the cell. In five additional experiments where aldosterone produced no significant stimulation of H+ transport, no change was noted in any of the metabolic or transport characteristics measured, suggesting that the alterations discussed above are dependent on the stimulation of H+ transport by the hormone. These results, along with some thermodynamic considerations, suggest that the effect of aldosterone is primarily exerted on the transport process rather than on metabolism. Further, it appears that prolonged stimulation of transport work leads to secondary alterations in the metabolic pathways reminiscent of the changes that occur in skeletal muscles of athletes undergoing physical conditioning.
Caution and Coronary Artery Surgery
Authors: CHARLES K. FRIEDBERG
Journal: Circulation (1972)

Timeo chirurgos et dona ferentes C ORONARY BYPASS surgery is un- doubtedly the current rage in cardiolog- ic practice, the major topic in cardiologic discussion.In his Presidential address to the American Heart Association, appearing in this issue of CIRCULATION, a distinguished cardiac surgeon urges caution in the application of the operation and calls for better definition of operative indications.Yet, even in the few months that have elapsed since the address was delivered, there has been a continuing and explosive increase in the number of such operations; it is estimated that, of approxi- mately 50,000 cardiac operations performed in the United States in the past year, 25,000 were for coronary artery disease.Is this growing popularity of the operation deserved?Is the enthusiasm of the surgeons who espouse and perform it warranted?Popularity of a new therapeutic procedure is no guarantee of its merit.Although history relates that a new idea is likely to be opposed and assailed a new treatment is rapidly and warmly embraced.This occurs particularly when available therapy, such as the medical management of angina pectoris, is unsatisfactory, and, as in other conditions, when
Differential Effects of a Segment of Slow Conduction on Reentrant Ventricular Tachycardia in the Rabbit Heart
Authors: Kai Haberl, Maurits Allessie
Journal: Circulation (1999)

Background —The purpose of this study was to compare differential effects of a segment of slow conduction during ventricular tachycardia (VT) due to depression of the action potential and electrical uncoupling. Methods and Results —In 33 Langendorff-perfused rabbit hearts, a ring of anisotropic left ventricular subepicardium was created by a cryoprocedure. Reentrant VT was produced by incremental pacing. Slow conduction in a segment of the ring was created by selective perfusion of the LAD with 10 mmol/L potassium or 0.75 mmol/L heptanol. As a result, VT cycle length increased from 193±34 to 235±37 ms (potassium) and 227±42 ms (heptanol). Reset curves were made by applying premature stimuli proximal to the area of depressed conduction. In a ring of uniform anisotropic tissue, the reset curve was almost completely flat. Electrical uncoupling of part of the ring (nonuniform anisotropy) resulted in a mixed reset curve. In both substrates, early premature beats failed to terminate VT. Depression of part of the ring by increasing K + resulted in a completely sloped reset curve, indicating a gap of partial excitability. Under these conditions, in 19 of 24 hearts, premature beats terminated VT by conduction block in the high K + area. Conclusions —The nature of the area of slow conduction determines the type of reset response and the ability to terminate VT.
Should Epileptics Scuba Dive?
Authors: R. Kelly Hill
Journal: JAMA (1985)

<h3>To the Editor.—</h3> Dr Dreifuss<sup>1</sup>raises an intriguing question in his letter concerning scuba diving and epilepsy, namely, Does a known epileptic have the right to participate in dangerous activities when he will be responsible for others? In general, I concur with his statement that the individual should be allowed to undertake those activities whose risks he believes are reasonable for himself alone. With respect to scuba diving, I completely agree with Dr Dreifuss' feelings concerning an epileptic as a diving instructor, but I think the same concerns apply to any diver. Even if the well-documented increased occurrence of seizures in a hyperbaric environment is ignored, the rationale that scuba diving by an epileptic is simply the assumption of personal risk is not valid. One of the primary safety procedures in scuba diving is the "buddy system," where divers are responsible for assisting each other in the event of
The effectiveness and safety of short‐contact dithranol therapy in paediatric psoriasis: a prospective comparison of regular day care and day care with telemedicine
Authors: A.M. Oostveen, C.A. Beulens, P.C.M. Kerkhof, E.M.G.J. Jong, M.M.B. Seyger
Journal: British Journal of Dermatology (2013)

Evidence on the effectiveness and safety of short-contact dithranol therapy in paediatric psoriasis is sparse and based only on retrospective data. The best results are achieved in a time-consuming day-care setting.To study prospectively the effectiveness and safety of short-contact dithranol therapy in paediatric psoriasis. In addition, the effectiveness, safety, duration of treatment and number of visits between regular day care and day care with telemedicine were compared.Data were collected from the prospective observational Child-CAPTURE registry of children with psoriasis. Effectiveness was measured as the mean percentage improvement in Psoriasis Area and Severity Index (PASI). Safety was assessed by recording adverse events. The number of visits and duration of treatment were reported.For all patients a mean percentage reduction in PASI score of -69·3% was found, with no significant differences between regular day care and day care with telemedicine. The only adverse event reported was irritation of the skin. Neither the frequency of irritation during treatment nor the mean duration of treatment significantly differed between the two groups. Patients with telemedicine had significantly fewer visits.This first prospective observational study demonstrates that short-contact dithranol therapy in paediatric psoriasis is effective and safe. Regular day care and day care with telemedicine are equally effective. Telemedicine can be of additional value as it is less time consuming. We hope it will therefore make dithranol treatment appropriate for a larger number of children with psoriasis.
Polyps of the rectum and colon
Authors: F. Potet, J. Soullard
Journal: Gut (1971)

Four hundred and thirty-three patients with adenomatous polyps were examined and followed up. It was found that well differentiated adenomas are stable but dedifferentiated polyps can lead to invasive cancer, usually over a long period of time. Thus the concept of malignant transformation becomes meaningless, and should be replaced by an initial histological evaluation of polyps of the rectum and colon so that their development can be predicted.
Effect of pitavastatin on type 2 diabetes mellitus nephropathy in KK-Ay/Ta mice
Authors: Masakazu Matsumoto, Mitsuo Tanimoto, Tomohito Gohda, Tatsuya Aoki, Maki Murakoshi, Kaori Yamada, Takahiko Yamazaki, Shigeru Kaneko, Satoshi Horikoshi, Yasuhiko Tomino
Journal: Metabolism (2008)
Clinical outcome after dynamic cardiomyoplasty for treatment of heart failure due to idiopathic dilated cardiomyopathy or Chagas's disease
Authors: Edimar Bocchi, Luis F. Moreira, Giovanni Bellotti, Antonio P. Barreto, Noedir Stolf, Adib Jatene, Fulvio Pileggi
Journal: Journal of the American College of Cardiology (1991)
Challenges in Systematic Reviews: Synthesis of Topics Related to the Delivery, Organization, and Financing of Health Care
Authors: Dena M. Bravata
Journal: Annals of Internal Medicine (2005)

Some important health policy topics, such as those related to the delivery, organization, and financing of health care, present substantial challenges to established methods for evidence synthesis. For example, such reviews may ask: What is the effect of for-profit versus not-for-profit delivery of care on patient outcomes? Or, which strategies are the most effective for promoting preventive care? This paper desc ribes innovative methods for synthesizing evidence related to the delivery, organization, and financing of health care. We found 13 systematic reviews on these topics that described novel methodologic approaches. Several of these syntheses used 3 approaches: conceptual frameworks to inform problem formulation, systematic searches that included nontraditional literature sources, and hybrid synthesis methods that included simulations to address key gaps in the literature. As the primary literature on these topics expands, so will opportunities to develop additional novel methods for performing high-quality comprehensive syntheses.
Nuclear factor κB up-regulation of CCAAT/enhancer-binding protein β mediates hepatocyte resistance to tumor necrosis factor α toxicity
Authors: Yongjun Wang, Rajat Singh, Youqing Xiang, Linda E. Greenbaum, Mark J. Czaja
Journal: Hepatology (2010)

The sensitization of hepatocytes to cell death from tumor necrosis factor α (TNFα) underlies many forms of hepatic injury, including that from toxins. Critical for hepatocyte resistance to TNFα toxicity is activation of nuclear factor κB (NF-κB) signaling, which prevents TNFα-induced death by the up-regulation of protective proteins. To further define the mechanisms of hepatocyte sensitization to TNFα killing, immunoblot analysis comparing livers from mice treated with lipopolysaccharide (LPS) alone or LPS together with the hepatotoxin galactosamine (GalN) was performed to identify TNFα-induced protective proteins blocked by GalN. Levels of CCAAT/enhancer-binding protein β (C/EBPβ) were increased after LPS treatment but not GalN/LPS treatment. In a nontransformed rat hepatocyte cell line, TNFα-induced increases in C/EBPβ protein levels were dependent on NF-κB-mediated inhibition of proteasomal degradation. Pharmacological inhibition of c-Jun N-terminal kinase (JNK) did not affect C/EBPβ degradation, indicating that the process was JNK-independent. C/EBPβ functioned to prevent cell death as adenoviral C/EBPβ overexpression blocked TNFα-induced apoptosis in cells sensitized to TNFα toxicity by NF-κB inhibition. C/EBPβ inhibited TNFα-induced caspase 8 activation and downstream mitochondrial cytochrome c release and caspase 3 and caspase 7 activation. Studies in primary hepatocytes from c/ebpβ(-/-) mice confirmed that loss of C/EBPβ increased death from TNFα. c/ebpβ(-/-) mice were also sensitized to liver injury from a nontoxic dose of LPS or TNFα. The absence of jnk2 failed to reverse the GalN-induced block in C/EBPβ induction by LPS, again demonstrating that C/EBPβ degradation was JNK-independent.
Abstract 2134: Unique and redundant roles of human RecQ homologs in cellular response to oxidative DNA damage
Authors: Sudha Sharma, Pornima Phatak, Alexei Stortchevoi, Jeanine LaRocque, Maria Jasin
Journal: Cancer Research (2012)

Abstract RecQ helicases contribute diverse activities towards genome maintenance in response to a variety of DNA lesions. Human RecQ homologs include RECQ1, BLM, WRN, RECQL4, and RECQ5α. Although these RecQ proteins are similar in their catalytic core and share certain biochemical properties in vitro, mutations in BLM, WRN and RecQ4 lead to clinically distinct diseases of cancer predisposition. This suggests that each human RecQ protein functions in distinct molecular events, but their specialized functions are only vaguely understood. RECQ1 is the most abundant but poorly characterized RecQ homolog in humans. Biochemically, RECQ1 displayed distinct substrate specificities from WRN and BLM, indicating that these helicases likely perform non-overlapping functions. Cellular studies imply that RECQ1 is involved in cellular proliferation and maintenance of genomic stability. We have obtained key preliminary evidence suggesting a unique role of RECQ1 in repair of oxidative DNA damage. RECQ1 is quickly recruited to the chromatin when cells are exposed to hydrogen peroxide (H2O2). Remarkably, the chromatin localization of RECQ1 is more robust and rapid than that of WRN helicase which has been shown to function in oxidative DNA damage repair. Deficiency in WRN or BLM helicase result in reduced homologous recombination and over-activation of PARP under basal condition; however, RECQ1-deficiency did not lead to PARP activation in undamaged cells and resulted in a comparatively modest, but significant, reduction in relative homologous recombination repair. In stark contrast to what is seen in WRN-deficiency, RECQ1-depleted cells over-activate PARP in a specific response to H2O2 treatment. Nonetheless, similar to WRN, RECQ1 associates with PARP-1 in human cells. Our results suggest a novel and non-overlapping role of RecQ1 in exogenously induced-oxidative DNA damage repair via modulation of PARP-1. Given that several RecQ proteins exhibit interaction with PARP-1, this study should provide a paradigm to delineate specialized and redundant functions of human RecQ homologs in DNA repair mechanisms. 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 2134. doi:1538-7445.AM2012-2134
TREATMENT OF MENINGOCOCCIC MENINGITIS WITH SULFONAMIDES
Authors: HORACE L. HODES
Journal: JAMA (1942)

Early in 1937 Schwentker, Gelman and Long 1 described the use of sulfanilamide in the treatment of 10 patients with meningococcic meningitis at Sydenham Hospital. Nine of the 10 patients treated recovered. Many other reports confirming the value of this drug in meningococcic meningitis have appeared. 2 It soon became apparent that sulfanilamide was at least as effective in meningitis as antimeningococcus serum. In fact, all the evidence points to the conclusion that the drug is more reliable than serum. For example, in Waghelstein's 3 series reported from Sydenham Hospital in 1938 the mortality rate in a series of 368 serum treated patients was 27 per cent, while among 72 patients receiving sulfanilamide the fatality rate was 15 per cent. As each new sulfonamide drug became available it was employed in meningococcic infections. During the past two years it has become evident that sulfapyridine, 4 sulfathiazole 5 and sulfadiazine 6
Uterine sarcomas: Review of 26 years at The Instituto Nacional de Cancerologia of Mexico
Authors: David Cantú de León, Heliodoro González, Delia Pérez Montiel, Jaime Coronel, Carlos Pérez-Plasencia, Verónica Villavicencio-Valencia, Ernesto Soto-Reyes, Luis Alonso Herrera
Journal: International Journal of Surgery (2013)
695. Cooperative Effects of Adenoviral Vector-Mediated Interleukin 12 Gene Therapy and Radiotherapy in a Preclinical Model of Metastatic Prostate Cancer
Authors: Tetsuo Fujita, Terry L. Timme, Koji Naruishi, Nobuyuki Kusaka, Julie X. Zhu, Guang Yang, Alexei Goltsov, Chenghui Ren, Chengzhen Ren, Maria T. Vlachaki, Bin S. Teh, E. Brian Butler, Timothy C. Thompson
Journal: Molecular Therapy (2005)

Introduction and Objective: The purpose of this study was to explore the potential benefits of combining adenoviral vector-mediated murine interleukin 12 (AdmIL-12) gene therapy with irradiation (XRT) in a subcutaneous metastatic prostate cancer model.
Abstract 2825: Characterization of a novel small molecule antagonist of 6-phosphofructo-2-kinase that suppresses glucose metabolism and tumor growth
Authors: Brian Clem, Gilles H. Tapolsky, Julie O'Neal, Pooran Chand, Amy Clem, John Trent, Sucheta Telang, Jason Chesney
Journal: Cancer Research (2011)

Abstract Over-expression of HIF-1α, activation of Ras and loss of p53 tumor suppressor function are associated with the development of human cancers and each of these genetic alterations converge on glycolysis by activating the 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFB). The PFKFB enzymes interconvert fructose-6-phosphate (F6P) and fructose-2,6-bisphosphate (F2,6BP) and F2,6BP is an allosteric activator of 6-phosphofructo-1-kinase (PFK-1), a rate-limiting enzyme and control point in the glycolytic pathway. There are four PFKFB family members which are encoded by separate genes (PFKFB1-4) and characterized by distinct kinase:bisphosphatase ratios. The PFKFB3 family member is of particular interest since it has been found to be activated in human cancer cell lines and tumors, to be increased by hypoxic exposure via HIF-1α and by oncogenic Ras, and to be required for tumorigenic growth. We recently discovered a competitive antagonist of PFKFB3 (3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one [3PO]) that reduces the glucose uptake, F2,6BP, lactate secretion, steady-state concentration of ATP, and growth of multiple transformed cell lines. Using a rationale design based approach, we have synthesized derivatives of 3PO and identified a compound (PFK-015) that: (i) more potently inhibits recombinant PFKFB3 (IC50:110 nM); (ii) inhibits PFKFB3 activity in cancer cells (IC50: 20 nM); (iii) is not a Pgp substrate as determined by transport and cell permeability assays in Caco-2 and MDCK-MDR1 (Papp A-B / B-A results 1.8 / 4 and 5 / 5 10−6 cm/s); (iv) inhibits cancer cell proliferation in a panel of 17 cancer cell lines; and (v) suppresses glucose uptake in cancer cells. Rodent PK studies following IV dosing at 5 mg/kg resulted in a profile with a satisfactory half-life (5.1 hours), exposure (AUCinf 1804 ng.h/ml), tissue distribution (Vd 20.5 L/kg) and reasonable clearance (46.2 mL/min/kg). Also, pre-clinical efficacy studies of C57Bl/6 mice bearing Lewis Lung Carcinoma (LLC) xenografts demonstrated ∼80% tumor growth inhibition relative to vehicle control. Finally, micro-PET studies performed on mice bearing LLC tumors showed a significant inhibition of tumor 2-[18F]-fluoro-2-deoxy-glucose uptake. These studies demonstrate that PFK-015 is an effective inhibitor of PFKFB3, possesses compelling in vitro properties, has satisfactory PK properties in rodents, and suppresses tumor glucose metabolism and growth in an aggressive mouse model of non-small cell lung cancer. These results support further development of PFK-015 as a novel anti-cancer agent. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2825. doi:10.1158/1538-7445.AM2011-2825
Haemolytic-Uraemic Syndrome in Typhoid Fever
Authors: N. M. Baker, A. E. Mills, I. Rachman, J. E. P. Thomas
Journal: BMJ (1974)

Among 48 patients with a typhoid infection 6 (12.5%) developed the haemolytic-uraemic syndrome. Neither glucose-6-phosphate dehydrogenase deficiency nor therapy with chloramphenicol could be incriminated as the causal factor. Evidence presented here suggests that the mechanism is localized intravascular coagulation.The presence of leucocytosis in typhoid fever suggests a complication and should alert one to the possibility of the haemolytic-uraemic syndrome. Furthermore, in our area typhoid should be suspected as a cause in any patient presenting with acute renal failure.
Brief Rhythmic Discharges in Electroencephalography on an Interictal to Ictal Continuum—Reply
Authors: Nicolas Gaspard, Ji Yeoun Yoo, Lawrence J. Hirsch
Journal: JAMA Neurology (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal