tbuckley/cabot-search huggingface dataset:
Abstract 16041: Beneficial Effects of Chronic Statin Pretreatment on Long-Term Prognosis in Patients With Acute Myocardial Infarction
Authors: Katsuomi Iwakura, Atsunori Okamura, Yasushi Koyama, Motoo Date, Koichi Inoue, Hiroyuki Nagai, Yuko Toyoshima, Koji Tanaka, Takafumi Oka, Nobuaki Tanaka, Yuko Yamanaka, Tomohiro Yamasaki, Tomoaki Okada, Yohei Sotomi, Kohei Azuma, Yoshiyuki Orihara, Satoshi Kameda, Mutsumi Iwamoto, Yoshihiro Ohta, Kenshi Fujii
Journal: Circulation (2014)

Introduction: Chronic administration of statins before onset of acute myocardial infarction (AMI) has protective effects on coronary microcirculation and reduces the infarct size irrespective of presence of dyslipidemia. It is not well elucidated whether the beneficial effects of statin pretreatment would be persistent on the chronic stage of infarction.

Hypothesis: The protective effect of pretreatment of statin could be associated with the improvement of long-term prognosis after AMI.

Methods: Among consecutive 803 patients with AMI who admitted between April 2004 and September 2012, we followed up 746 patients (age: 64±13 years, male: 82.4%) whose clinical history including medication before administration was confirmed. The primary endpoint was all-cause death.

Results: Statins were administered in 112 patients (15.0%) before hospital administration for AMI. Patients with pretreatment of statins had significantly lower peak CK (2248±2008 vs. 3400±3663 IU/L, p=0.001) and CK-MB (153±126 vs. 245±390 IU/L, p=0.001) than those without it. The median of the follow-up period was 1026 days (range: 2 - 2024 days), and we observed all-cause death in 62 patients (8.3%) during that period. Kaplan-Meier survival curve analysis demonstrated that statin pretreatment was associated with better survival rate over the follow-up period (p= 0.018 by logrank test) (Figure). Patients receiving statin pretreatment had lower mortality among those with dyslipidemia (n=429, p=0.008), and tended to have it among those receiving statins at hospital discharge (n=396, p= 0.053).

Conclusions: Chronic pretreatment of statins before AMI onset was associated not only with smaller infarct size but also with better long-term survival.

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Abstract 164: Sodium Nitroprusside Improves Carotid Blood Flow and 24-Hour Neurological Intact Survival in a Porcine Model of Prolonged CPR.
Authors: Demetris Yannopoulos, Timothy Matsuura, Scott McKnite, Tom Aufderheide, Menekhem Zviman, Henry Halperin, Keith G Lurie
Journal: Circulation (2010)

Introduction:  Sodium nitroprusside (SNP) is a powerful vasodilator. In an effort to improve vital organ blood flow during CPR and optimize microcirculation, we tested the hypothesis that high doses of SNP would be beneficial for treating cardiac arrest when administered with devices and techniques known to enhance blood pressure and circulation during CPR.   Methods:  Twenty one (30±1Kg) pigs, intubated and isofluorane anesthetized, had 6 minutes of untreated ventricular. Group A: 5 animals received standard (S-) cardiopulmonary resuscitation (CPR). Group B: 8 received active compression decompression (ACD) CPR plus an inspiratory impedance threshold device (ITD) plus abdominal binding (AB). Group C: 8 received ACD+ITD+AB+SNP CPR for 25 minutes before defibrillation was attempted. SNP (1mg iv) was given every 5 minutes. Animals in groups A and B received epinephrine based on the 2005 AHA guidelines before defibrillation. Right atrial, aortic pressure and carotid blood flow were recorded. Successfully resuscitated animals were recovered and evaluated 24 hours later for cerebral performance category score. Statistical comparisons were performed by ANOVA and Fisher9s exact test.   Results:  Systolic/diastolic pressures (mmHg) were significantly higher in groups B and C compared to A (mean± SD: 82±7/34±3 and 78±11/38±5 vs 42±6/18±5, respectively,    Conclusions:  SNP can safely be used in pigs to significantly improve vital organ perfusion and 24 hour survival when used in conjunction with ACD CPR+ITD+AB. This mechano-pharmacological therapy maintains vital organ viability during prolonged CPR.
Abstract 899: High fat diet induced DNA methylation at transcription factor binding region and repressed gene expression of a metastasis suppressor E-cadherin in primary site of murine metastatic breast cancer (MBC), and promoted invasion of MBC cells to lung and liver
Authors: Yukun Zhang, Wendan Wang, Xujuan Yang, William G. Helferich
Journal: Cancer Research (2015)

Abstract Breast cancer (BC) is the most prevalent type of cancer among women in the US. BC survival rate has long been compromised by metastasis. Consumption of a high fat diet (HFD) is associated with increased BC risk. However, the underlying molecular mechanisms remain inconclusive. E-cadherin (Cdh1) is a metastasis suppressor, the loss of which promotes tumor invasion. We aimed to examine the effects of a HFD containing 47% kcal from fat on metastatic breast cancer (MBC) using preclinical syngeneic mouse models. To access the dietary effect on metastatic mammary tumor, we injected MBC cells into the mammary duct of BALB/c mice. To evaluate the dietary effect on the spread of MBC from bone to lung and liver tissues, MBC cells were inoculated into tibia cavity of BALB/c mice. Growth of MBC at the injection and inoculation site, and invasion of MBC to other organs were monitored in real-time by the bioluminescence imaging (BLI) system. Three weeks post injection, animals were sacrificed and tissues samples were collected. In summary, our results showed that HFD promoted the invasion of MBC cells to lung and liver of mice. H&amp;E staining showed that there were significantly more lung tumors in the HFD group than control group in the tibial injected animals (12.9±1.6, 8.9±1.1, P&amp;lt;0.05), as well as more mice with liver tumors in HFD group (7 out of 16 mice with liver tumors in HFD group, 0 out of 17 mice with liver tumors in control group). Expression of Cdh1mammary tumor of mice was decreased by HFD. Intensity of methylation at the CpG-rich promoter region, where transcription factors bind, was increased by HFD in the mammary tumor. As the first to report that HFD induced DNA methylation and decreased the expression of Cdh1 in the metastatic mammary tumor, we proposed a mechanism by which HFD enhanced the invasiveness of MBC. Having laid a base and provided clues on HFD and MBC, this study also shed light on the intriguing interactions of nutrient epigenome and BC. Future studies are needed to further extrapolate our findings into the link between diet and disease in BC patients. Citation Format: Yukun Zhang, Wendan Wang, Xujuan Yang, William G. Helferich. High fat diet induced DNA methylation at transcription factor binding region and repressed gene expression of a metastasis suppressor E-cadherin in primary site of murine metastatic breast cancer (MBC), and promoted invasion of MBC cells to lung and liver [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 899. doi:10.1158/1538-7445.AM2015-899
Nova et Vetera
Authors: F T CROSSLING
Journal: BMJ (1961)

NEW APPLIANCES MBICTJOUL be easily replaced after removing the two cross-bars.The " U " bottom is thought to be better than the conventional peg end.Such a crutch can be made at any hospital in a matter of minutes with a minimum of equipment.This pattern has been adopted by the Uganda Medical Service and the Mulago Round Table Polio Clinic.The diagram was drawn by Mr. Peter Gull.
Abstract 5492: Tetrahydrobiopterin (BH4) Improves Endothelial Cell Survival After Vascular Injury
Authors: Ruth Rinze, Ziad A Ali, Gillian Douglas, Nicholas J Alp, Keith M Channon
Journal: Circulation (2008)

Endothelial cell loss, survival and regeneration are important aspects of the response to vascular injury leading to neointimal hyperplasia and accelerated atherosclerosis. Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a key regulator of endothelial cell biology and has been shown to prevent endothelial cell apoptosis. The cofactor tetrahydrobiopterin (BH4) is essential for eNOS catalytic activity but its impact on endothelial cell survival and regeneration remains unclear. We investigated the effect of BH4 on endothelial cell survival and vascular remodelling using ApoE-KO mice with transgenic endothelial-targeted overexpression of GTP cyclohydrolase 1 (GCH), the rate limiting enzyme of BH4 synthesis, and with endothelial specific transgenic expression of the LacZ reporter gene. Using venous bypass grafts as an in vivo model of acute vascular injury, we observed that endothelial-specific augmentation of BH4 in GCH/ApoE-KO mice improved survival of vein graft-derived endothelial cells and reduced neointimal hyperplasia. To address the hypothesis that augmentation of BH4 increases the capacity of endothelial cells from GCH/ApoE-KO mice to survive vascular injury, we cultured primary lung endothelial cells from mice expressing the GCH transgene and wild type littermates. Endothelial cells, isolated by immunomagnetic beads, were positive for CD31, CD102 and Tie2. Protein levels of eNOS were not different between wild type and GCH mice. BH4 levels were selectively increased in pulmonary endothelial cells from GCH mice, &gt; 10-fold, compared with a 3-fold increase in total lung tissue BH4. There was no difference in total lung endothelial cell content or amount of isolated cells between ApoE-KO and GCH/ApoE-KO mice, determined by Tie2-driven β-galactosidase activity. However, after 3 days of culture both total endothelial cell number and number of endothelial cell colonies in GCH/ApoE-KO were significantly increased (236% ± 47 p=0.028 and 195% ± 28 p=0.014 respectively, n=5) whereas mean colony size remained unchanged. These observations indicate an important role for BH4 in endothelial cell survival and endothelial regeneration, and identify BH4 as a potential therapeutic target in vascular injury states.
Rehabilitation of Traumatic and Orthopaedic Patients
Authors: G. C. Fletcher, V. H. Wheble
Journal: BMJ (1964)

In 1935 a committee of the British Medical Association made a report on the treatment of fractures in which the results of treating cases in fracture clinics under the care of orthopaedic surgeons were compared with results obtained by other means, particular notice being taken of the decrease in time off work. No one who has studied this report could fail to be convinced of the effectiveness of fracture clinics in hospitals. In addition, however, the Committee suggested something which was quite new at the time. It recommended that rehabilitation centres should be established in each industrial area. Under the Disabled Persons (Employment) Act 1944 the Government has provided something of this nature in the form of industrial rehabilitation units in various parts of the country, particularly where there are high concentrations of industry. These units have, however, in the past been used mainly for the rehabilitation of patients who have been off work for long periods. Yet it has been shown by Plewes et al. (1948), using a special unit in the Vauxhall Motor Works at Luton, that better results can be obtained if industrial rehabilitation is begun as soon as possible after an injury or other disability. Here the conditions were ideal in that the patients passing through the rehabilitation units were from one large industrial organization and were dealt with from the medical and financial point of view by their own management. Plewes et al. recom mended that group industrial rehabilitation centres should be based on up-to-date and well-staffed hospitals where facilities for diagnosis and prompt surgical treatment are present.
Child psychiatry fellowship training: a crisis in recruitment and manpower
Authors: E V Beresin, J F Borus
Journal: American Journal of Psychiatry (1989)

Eighty-three percent (104 of 126) of the accredited child psychiatry fellowships in the United States responded to a survey of current manpower and training problems facing child psychiatry. Thirty-five percent of the respondents were having trouble filling their classes with highly qualified fellows, and 45% were having difficulty recruiting faculty child psychiatrists. Other significant problems included developing faculty interest in research, providing didactic seminars in new areas such as developmental neurobiology and infant psychiatry, and funding fellow and faculty positions and research. The authors examine this crisis in manpower, recruitment, and training and suggest solutions on local and national levels.
Risk of New or Recurrent Cancer in Patients With Inflammatory Bowel Disease and Previous Cancer Exposed to Immunosuppressive and Anti-Tumor Necrosis Factor Agents
Authors: Jordan Axelrad, Oren Bernheim, Jean-Frederic Colombel, Stefano Malerba, Ashwin Ananthakrishnan, Vijay Yajnik, Gila Hoffman, Manasi Agrawal, Dana Lukin, Amit Desai, Elisa McEachern, Brian Bosworth, Ellen Scherl, Andre Reyes, Hina Zaidi, Prashant Mudireddy, David DiCaprio, Keith Sultan, Burton Korelitz, Erwin Wang, Renee Williams, LeaAnn Chen, Seymour Katz, Steven Itzkowitz
Journal: Clinical Gastroenterology and Hepatology (2015)
Abstract 17160: Vagolytic Therapy Prevents CPVT Induction in Casq2-KO Mice
Authors: Michela Faggioni, Hyun Seok Hwang, Christian van der Werf, Bjorn C Knollmann
Journal: Circulation (2011)

Background: Cathecolaminergic polymorphic ventricular (CPVT) is characterized by an increase in the ventricular arrhythmia burden with a gradual rise in the heart rate. However it has been observed that in young patients reaching maximum heart rate during exercise test CPVT may paradoxically be abolished. In addition, we previously reported that in isolated Casq2-/- hearts, a CPVT mouse model, an increase in heart rate can prevent the induction of CPVT. Here we hypothesize that increasing heart rate by vagolytic therapy can prevent CPVT in vivo. Methods: Surface ECGs were recorded from 11 anaesthetized Casq2-/- mice (4 males and 7 females; 24±2 month of age). Vagolytic therapy was performed with an i.p. injection of 0.5mg/kg of atropine. After the heart rate increase had reached its plateau (~10 min post atropine), catecholamine challenge was carried out with 1.5mg/kg isoproterenol (Atr/ISO group). The incidence of PVC and VT was analyzed and compared with that obtained in the same mice after injection of only 1.5mg/kg of isoproterenol (ISO group). Results: Administration of atropine in Casq2-/- mice increased the heart rate by 23% (±4%) but did not induce any arrhythmia (Fig. A). On the other hand, ISO alone, as expected, caused PVCs in all mice and VT episodes in 4/11 mice. Pretreatment with atropin significantly reduced PVC incidence during ISO challenge (Atr/ISO: 1.13±0.46 PVC/min vs. ISO: 4.93±1.74 PVC/min, p&lt;0.05) (Fig. B) and completely prevented VT induction. Conversely, slowing the sinus heart by infusion of the muscarinic agonist carbachol significantly increased the incidence of ISO-induced CPVT in isolated perfused Casq2-/- hearts (n = 20 hearts, p&lt;0.01). Conclusions: A catecholamine-independent increase in the sinus heart rate, obtained by muscarinic receptor block with atropine, is sufficient to protect Casq2-KO mice from CPVT during catecholamine challenge in vivo.
Surveillance Systems to Track Progress Toward Polio Eradication — Worldwide, 2014–2015
Authors: Cynthia J. Snider, Ousmane M. Diop, Cara C. Burns, Rudolph H. Tangermann, Steven G.F. Wassilak
Journal: MMWR Morbidity and Mortality Weekly Report (2016)

Global efforts to eradicate polio began in 1988, and polio-free certification has been achieved in four of the six World Health Organization (WHO) regions. Nigeria was removed from WHO's list of countries with endemic polio in September 2015, achieving an important milestone toward interruption of wild poliovirus (WPV) transmission in the African Region (1). Afghanistan and Pakistan, both in the Eastern Mediterranean Region, were the only countries to report WPV cases in 2015. Previously reported outbreaks caused by WPV importation during 2013-2014 have ended (2,3). The primary means for detecting poliovirus transmission is surveillance for acute flaccid paralysis (AFP) among children aged <15 years (4,5). Stool specimens collected from children with AFP are tested for both WPV and vaccine-derived poliovirus (VDPV) in WHO-accredited laboratories within the Global Polio Laboratory Network (GPLN). In selected locations, AFP surveillance is supplemented with environmental surveillance (testing sewage for poliovirus) (6). Testing of stool and sewage samples includes genomic sequencing to characterize poliovirus isolates; results are used to map poliovirus transmission and identify gaps in AFP surveillance. This report presents poliovirus surveillance data from 2014 and 2015, focusing on the 20 countries in the African Region and six in the Eastern Mediterranean Region that reported a WPV or circulating VDPV (cVDPV) case during 2011-2015, including Guinea, Liberia, and Sierra Leone, which were most affected by the 2014-2015 Ebola virus disease (Ebola) outbreak.
Infection with hepatitis C virus
Authors: N. Hallam, J. Kurtz, A. Dike, D. Parker
Journal: BMJ (1994)

Editor,--A recent editorial discussed screening for hepatitis C virus infection.1 During the first eight months of screening for hepatitis C virus in the Oxford region 83 177 units of blood (from 70 700 donors) were tested with the Ortho second generation enzyme linked immunoassay. These reactions were repeatedly positive in 358 (0.5% of all donors), and these were referred to the virology department for confirmation by the second generation recombinant immunoblot assay (RIBA-2, Ortho) and Murex BCJ11 enzyme linked immunoassay (with non-structural 5 and core antigens). Thirty nine samples (0.05% of all donors) were confirmed to be positive, reacting …
Peripheral blood mononuclear cells of a patient with advanced Hodgkin's lymphoma give rise to permanently growing Hodgkin-Reed Sternberg cells
Authors: J Wolf, U Kapp, H Bohlen, M Kornacker, C Schoch, B Stahl, S Mucke, C von Kalle, C Fonatsch, HE Schaefer, ML Hansmann, V Diehl
Journal: Blood (1996)
Gene-diet interactions in arginine-dependent intestinal carcinogenesis
Authors: Hagit Yerushalmi, Karen Blohm-Mangone, Philip Yamauchi, Jose Padilla-Torres, David G. Besselsen, Hui Zhang, Natalia Ignatenko, Hana Holubec, Claire M. Payne, Eugene W. Gerner
Journal: Cancer Research (2004)

3904  L-arginine, an essential amino acid, is converted by arginase to ornithine, the substrate for polyamine synthesis. Polyamines (putrescine, spermidine and spermine) are small ubiquitous molecules involved in various processes and required for cell proliferation. L-arginine is also metabolized by nitric oxide synthases (NOSs) to form nitric oxide (NO) that can influence signal transduction and DNA damage. NOSs are found as constitutively expressed isoforms (NOS1/NOS3) or the inducible isoform (NOS2). In this study, we evaluated NOS2 and dietary L-arginine effects on intestinal tumorgenesis in Min (multiple intestinal neoplasia) mice. Min mice were crossed with NOS2 knockout mice or wild-type NOS2 mice. NOS2 protein was expressed in small intestine, but not the colon, of Min X NOS2 (+/+) mice. The protein was not detected in either intestinal tissue of Min X NOS2 (−/−) mice. When animals were fed an arginine-restricted diet, loss of NOS2 alleles was associated with a small (50% or less) increase in small intestinal tumor number and colonic tumor incidence, compared to Min X NOS2 (+/+) mice. Supplemental arginine (up to 2% in the drinking water) slightly decreased small intestinal tumor number, in a concentration-dependent manner, in Min X NOS2 (−/−) mice. In mice expressing NOS2, intestinal tumor number was minimally affected by dietary arginine. In these mice, dietary arginine increased small intestinal arginine and ornithine contents, whereas in Min X NOS2 (−/−) mice no changes were observed. Colon tumor incidence showed an increase with dietary arginine, independent of NOS2 expression. This increase can result from dietary-arginine dependent increase in ornithine and putrescine contents. These data suggest that NOS2 expression and dietary arginine have only minimal effects on small intestinal carcinogenesis in the Min mouse. However, dietary arginine increases the incidence of colonic tumors, resulting from lack of expression of the adenomatous polyposis coli (APC) gene, by a NOS2-independent mechanism that may involve polyamines.
Abstract 3715: Survival of patients with mucinous ovarian carcinoma and ovarian metastases: A population-based cancer registry study
Authors: Michiel Simons, Nicole Ezendam, Johan Bulten, Iris Nagtegaal, Leon Massuger
Journal: Cancer Research (2015)

Abstract Objectives: Patients with mucinous ovarian carcinoma (MOC) generally have a favorable prognosis, although in advanced stage, prognosis is significantly worse compared to patients with serous ovarian carcinomas (SOC). This might be due to the difficulties in the distinction of MOC from metastatic tumors. In the current study we investigate prognosis of MOC compared to other types of ovarian cancer and to synchronous metastases to the ovary (sMO). Materials and methods: Age, laterality, FIGO stage, tumor grade, treatment and survival were extracted from the Eindhoven Cancer registry for all patients diagnosed with ovarian carcinomas or sMO between 1990 and 2012. 5-year survival analysis and Cox proportional hazard analysis were conducted. Results: 3,556 patients with primary ovarian carcinoma (of which 474 mucinous) and 289 with sMO were identified. In advanced stage, 5-year survival of patients with MOC was comparable to survival of patients with sMO (11% vs. 11%, p = 0.32) and decreased compared to patients with SOC (26%, p&amp;lt;0.01). For MOC there was no clinically significant effect on 5-year survival of either debulking (12% vs. 8%, p&amp;lt;0.01) or chemotherapy (12% vs. 10%, p = 0.02) as compared to patients with SOC (28 vs. 13% after chemotherapy, p&amp;lt;0.01 and 29% vs. 5% after debulking, p&amp;lt;0.01). Multivariate regression analysis for age, tumor grade and subtype including sMO was carried out, showing a significantly better overall survival for SOC compared to MOC (HR 0.51, p&amp;lt;0.01), whereas there was no difference for sMO compared with MOC (HR 1.16, p = 0.19). Conclusion: Patients with advanced stage MOC have a worse prognosis than advanced stage SOC. Survival is almost identical to that of patients with sMO, which might indicate that (a large part of) advanced stage MOC are in fact metastases. This may partly explain the limited effects of chemotherapy and debulking in patients with MOC. Methods to differentiate between primary MOC and metastatic disease are needed to provide optimal treatment and insight in prognosis. Citation Format: Michiel Simons, Nicole Ezendam, Johan Bulten, Iris Nagtegaal, Leon Massuger. Survival of patients with mucinous ovarian carcinoma and ovarian metastases: A population-based cancer registry study. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3715. doi:10.1158/1538-7445.AM2015-3715