tbuckley/cabot-search huggingface dataset:
Abstract 167: Growth Induction to Reverse Congenital Aortic Developmental Hypoplasia
Authors: Daniel F Labuz, James M Berry, Lee A Pyles, John E Foker
Journal: Circulation Research (2014)

Objectives: Congenital heart disease may include hypoplastic heart valves, ventricles or great arteries. Infants with coarctation of the aorta (CoA) often have a hypoplastic transverse aortic arch (TAA) which can greatly complicate surgical repairs. Although these defects are often considered to be genetic in origin, our hypothesis was that they are problems of development which are potentially reversible. We tested the corollary hypothesis that hypoplastic TAAs retain normal developmental potential and the increased aortic flow after CoA repair provides the biomechanical signal for catch-up growth. Methods: Infants (N = 19) with TAA hypoplasia who underwent surgical CoA repair were studied for TAA growth by echocardiography done prior to and at intervals up to 13 years later. The TAA diameters were indexed using nomograms and calculated as standard deviations from expected size (SDE). Normal range is ± 2 SDE and &lt; −2 indicates hypoplasia. Results: 1) TAA growth was rapid and significant within 3 months. 2) The initial average TAA SDE = −3.7 (range: −7.6 to −2.1) (0/19 normal); 3 months = −1.5 (-4.1 to 0.9) (12/17); 1 year = −1.0 (-4.2 to 1.3) (15/19); 5 to 13 years = −0.6 (-2.1 to 0.9) (16/17 normal). Conclusions: 1) Hypoplastic aortic arches grew rapidly to normal size with increased flow following CoA repair. 2) The results suggest the cause of hypoplasia was underdevelopment from low flow and, when increased, flow provided the biomechanical signal to induce catch up growth. 3) Infants were a relevant model for demonstrating the aortic growth signal. 4) Growth induction by increased blood flow could be used to reverse aortic underdevelopment in other selected patients.
A Phase 1 Study Of JNJ-40346527, a Colony Stimulating Factor-1 Receptor (CSF-1R) Inhibitor, In Patients With Relapsed Or Refractory Hodgkin Lymphoma
Authors: Bastian von Tresckow, Franck Morschhauser, Vincent Ribrag, Max S. Topp, Caly Chien, Shobha Seetharam, Regina Aquino, Sonja Kotoulek, Imran Khan, Carla de Boer, Andreas Engert
Journal: Blood (2013)
Pulmonary Tuberculosis in the Nigerian African
Authors: B. S. Jones
Journal: BMJ (1949)

DITLSOURNAL 781Other therapeutic applications in treating arterial emboli, reflex anuria, abdominal distension, and vascular insufficiency have been described.Continuous caudal analgesia has been determined of great value in the prognosis of sympathectomy for essential hypertension.It opens a new avenue for the prolonged control of post- operative and intractable pain in terminal carcinoniatosis.Finally, the medical profession and I personally express our gratitude to our European colleagues who in 1901, after careful researches, made possible this medical technique which it has been my privilege to extend into these various applications.
Abstract 13008: Reversal of Aging-Induced Upregulation of Cardiac Inducible Nitric Oxide Synthase and Beta-Adrenergic Desensitization in Mice Lacking the Beta3-Adrenoreceptor
Authors: Heng-Jie Cheng, Peng Zhou, Dalane W Kitzman, Stephen B Kritchevsky, David C Sane, William C Little, Che-Ping Cheng
Journal: Circulation (2010)

Background: We have shown previously that cardiac aging (CA) is associated with enhanced β3-adrenergic receptor (AR)-evoked inhibition of cardiomyocyte function accompanied by hyporesponsiveness to...
Abstract 3786: The Virtual Histology Intravascular Ultrasound Appearance of Newly-Placed Drug-Eluting Stents: Implications for Follow-up Analyses
Authors: Sang-Wook Kim, Gary S Mintz, Patrick Ohlmann, Young Joon Hong, Salah-Eddine Hassani, Aleksandra Michalek, Sundeep Mishra, Esteban Escolar, Rajbabu Pakala, Anh B Bui, Guy Weigold, Augusto D Pichard, Lowell F Satler, Kenneth M Kent, William O Suddath, Ron Waksman, Neil J Weissman
Journal: Circulation (2006)

Background. Intravascular ultrasound (IVUS) is used pre and post-intervention and at follow-up. IVUS Virtual Histology (VH) classifies tissue into fibrous, fibrofatty, dense calcium, and necrotic c...
Antitumor activity of a synthetic agonist of TLR9 in preclinical lung cancer models
Authors: D. Wang, D. Yu, E. R. Kandimalla, S. Agrawal
Journal: Journal of Clinical Oncology (2006)

2568 Background: Synthetic agonists of TLR9 induce potent Th1-type innate and adaptive immune responses. In the present study, we have studied antitumor activity of a synthetic agonist of TLR9 referred to as immune modulatory oligonucleotide (IMO) in lung cancer models either alone or in combination with chemotherapeutic agents. Methods: Two different models are evaluated. In one model, mice implanted peritoneally with 3LL-C75 lung carcinoma cells were administered with IMO or PBS once in every two days for six times for evaluating antitumor activity of IMO alone. In a second model, to evaluate combination treatment of IMO with Gemcitabine or cyclophosphamide, mice bearing subcutaneously implanted 3LL tumor were administered with peritumoral injections of IMO and i.p. injections of Gemcitabine or cyclophosphamide. Results and Conclusions: Administration of IMO to mice bearing 3LL-C75 lung carcinoma inhibited tumor growth. Tumor free mice from this study failed to grow tumor when rechallenged with 3LL-C75 lung carcinoma cells, suggesting tumor bearing mice administered with IMO developed memory responses for the same tumor. Further more, naïve mice adoptively transferred with splenocytes obtained from mice that remained tumor free from the above treatment group failed to grow tumor to a rechallenge with 3LL-C75 tumor cells. The co-administration of IMO with chemotherapeutic agents, Gemcitabine and cyclophosphamide resulted in enhanced antitumor effects in 3LL lung cancer model. The present studies show potent antitumor activity of IMO when administered alone and in combination with Gemcitabine and cyclophosphamide in preclinical lung cancer models. [Table: see text]
腹痛-双肾积水-蛋白尿
Authors: 黄晓明, 陈嘉林, 曾学军
Journal: BMJ (2008)

患者女，37岁。因“反复腹痛、腹泻、恶心呕吐2年”入院。患者于2004年7月无明显诱因出现脐周持续性绞痛，伴恶心、呕吐，呕吐物为胃内容物，无胆汁及宿食，无呕血及咖啡样物。腹痛同时出现腹泻，3-4次／d，糊状或水样便，无黏液脓血，便后腹痛可稍缓解。无发热。大便常规未见红细胞、白细胞。血常规白细胞4000／mm^3左右。
Cost offset from a psychiatric consultation-liaison intervention with elderly hip fracture patients
Authors: J J Strain, J S Lyons, J S Hammer, M Fahs, A Lebovits, P L Paddison, S Snyder, E Strauss, R Burton, G Nuber
Journal: American Journal of Psychiatry (1991)

The authors hypothesized that psychiatric liaison screening of elderly patients with hip fractures would shorten the average length of hospital stay and increase the proportion of patients who returned home after discharge.The study was performed at Mount Sinai Medical Center in New York and Northwestern Memorial Hospital in Chicago. The subjects were 452 patients 65 years or older who were consecutively admitted for surgical repair of fractured hips. During a baseline year the patients received traditional referral for psychiatric consultation. During the experimental year all the patients at Mount Sinai and the patients on one Northwestern Unit were screened for psychiatric consultation.The patients who received psychiatric liaison screening had a higher consultation rate than those who received traditional consultation. The rates of DSM-III disorders in the experimental year were 56% at Mount Sinai and 60% at Northwestern. The mean length of stay was reduced from 20.7 to 18.5 days at Mount Sinai and from 15.5 to 13.8 days at Northwestern, resulting in reductions in hospital costs ($647/day) of $166,926 and $97,361, respectively. Fees generated from Medicare service delivery could have paid for the $20,000 psychiatric intervention cost at each site. There was no difference, however, between the two years in the discharge placement of patients.Admission psychiatric liaison screening of elderly patients with hip fractures results in early detection of psychiatric morbidity, better psychiatric care, earlier discharge, and substantial cost savings to the hospital.
偏头痛的预防性治疗（β-受体阻滞剂）、行为治疗及二者联合使用对发作性偏头痛急性期优化治疗的疗效影响：一项随机对照试验
Authors: Kenneth, Holroyd, Gary, Eordingley, Ohio, 李力波, 管宇宙
Journal: BMJ (2011)

目的观察偏头痛的预防性治疗（β-受体阻滞剂）、短期行为治疗及二者联合使用能否增强发作性偏头痛急性期优化治疗的疗效。设计观察期为16个月的随机安慰剂对照实验，试验起止日期为2001年7月至2005年11月地点美国俄亥俄州2个门诊中心。
Prompt Immune Tolerance Induction at Inhibitor Diagnosis Regardless of Titer May Increase Overall Success in Hemophilia A With Inhibitors: Experience of Two US Centers
Authors: Charles T Nakar, Marilyn J. Manco-Johnson, Alice Lail, Sharyne M. Donfield, Jennifer Maahs, Young Chong, Taylor A Blades, Amy D. Shapiro
Journal: Blood (2013)
Abstract 17075: Preferential Targeting of Bnip3 Isoforms to Mitochondria or Endoplasmic Reticulum During Metabolic Stress Promotes Autophagy or Cell Survival of Post-Natal Ventricular Myocytes
Authors: Joseph W Gordon, Yan Wang, Yan Hai, Rimpy Dhingra, Hongying Gang, Lorrie A Kirshenbaum
Journal: Circulation (2011)

Autophagy is an evolutionary conserved process that allows cells to recycle or discard macromolecular constituents or damaged organelles during times of metabolic crisis. Alternative mRNA splicing is a versatile mechanism by which cells generate proteins with different or even antagonistic properties. Herein, we show that inclusion or skipping of exon3 of Bnip3 mRNA generates proteins with distinct and opposing actions on autophagy and cell survival. Metabolic stress imposed by hypoxia or nutrient deprivation resulted in the synthesis of two Bnip3 mRNA isoforms in post-natal ventricular myocytes in vitro and in vivo. Notably, one Bnip3 mRNA comprised of exons 1 through 6 encoded a protein of 26kDa, while a second mRNA generated by the fusion of exon2 and exon4 encoded a truncated Bnip3 protein of 8.2kDa. Sequence analysis revealed the truncated isoform encodes a conserved C-terminus domain that exclusively targets Bnip3 to the endoplasmic reticulum (ER) and not mitochondrion. While the 26kDa Bnip3 induced mitochondrial perturbations and autophagy, the spliced isoform suppressed Bnip3 induced mitochondrial defects and autophagy. Interestingly switching from glucose to fatty metabolism by supplementing nutrient deprived ventricular myocytes with carnitine but not pyruvate preferentially accumulated the spliced isoform of Bnip3 and the association of Bcl-2/Beclin-1 complexes at the ER, while suppressing autophagy. Furthermore, C-terminal domain mutations of the spliced variant defective for ER targeting sensitized cardiac myocytes to mitochondrial perturbations and apoptosis. To our knowledge our data provide the first direct evidence for a novel survival mechanism whereby the metabolic status of the cell programs autophagy or apoptosis by preferentially targeting Bnip3 isoforms to mitochondria or ER during metabolic stress.
Abstract 1477: Identification and Functional Analysis of Protein Interaction Partners of the Estrogen Receptor Alpha in the Human Heart
Authors: Shokoufeh Mahmoodzadeh, Hang Pham, Mercy M Davidson, Vera Regitz-Zagrosek
Journal: Circulation (2008)

Background and aims: Estrogens (E2) are important regulators of physiological and pathological processes in various target tissues, including the human heart. Most of the biological actions of E2 are mediated by nuclear steroid receptors, the estrogen receptor alpha (ERα) and beta (ERα), which function as hormone-inducible transcription factors. ERs act in concert with other regulatory elements to mediate estrogenic effects. So far, only few cofactors of ERs have been described in the human heart. To gain a better understanding of E2-mediated ERα action in the human heart, we identified and functionally analyzed the interaction partners of ERα. Methods: The yeast two hybrid screen (YTH) was performed in the presence of E2 with ERα as bait in a human heart cDNA library. Co-immunoprecipitation analysis (Co-IP) with human atrial proteins was carried out to confirm the interaction in a mammalian system. Immunofluorescence (IF) methods were employed on human atrial tissue samples as well as in cotransfected AC16 cells to analyze the co-localisation of ERα and its binding partners. Promoter reporter assays were performed to show the regulation of the identified interaction partner by ERα. Results: Yeast two hybrid screening of a human heart library revealed that ERα interacts with the atrial natriuretic peptide precursor A (NPPA). Retransformation experiments showed that NPPA can interact with ERα full-length and the ERα-EF domain in an E2-dependent manner. The LxxLL-motif of NPPA was found to interact with the ERα-EF domain in yeast. The interaction of NPPA and ERα was also confirmed using proteins derived from human atrium by Co-IP. IF analysis showed that E2 treatment of AC16 cells led to an increased translocation of NPPA and ERα in the nucleus of AC16 cells and also their co-localization there. Furthermore, expression analysis with NPPA luciferase promoter constructs showed a significant increase in the promoter activity in the presence of E2/ERα. Conclusion: We showed the interaction of ERα and NPPA in an E2-dependent manner. Our findings suggest that the E2-activated ERα and NPPA complex binds to specific regions on the NPPA promoter leading to transcriptional regulation of the NPPA gene.
Diagnosis of Occult Melanoma Using Transient Receptor Potential Melastatin 1 (TRPM1) Autoantibody Testing
Authors: Monica D. Dalal, Catherine W. Morgans, Robert M. Duvoisin, Elizabeth A. Gamboa, Brett G. Jeffrey, Sunir J. Garg, Chi-Chao Chan, H. Nida Sen
Journal: Ophthalmology (2013)
Abstract P4-05-01: Genetic analysis of the role of Brca1 in suppression of basal-like breast cancer
Authors: Xin-Hai Pei, Feng Bai, Ho Lam Chan, Alexandria Scott, Matthew D Smith, Cheng Fan, Jason I Herschkowitz, Charles M Perou, Alan S Livingstone, David J Robbins, Anthony J Capobianco
Journal: Cancer Research (2015)

Abstract BRCA1 mutation carriers are predisposed to developing basal-like breast cancers with high metastasis and poor prognosis. However, the mechanism underlying the function of BRCA1 in suppressing basal-like breast cancer remains unclear. We previously reported that deletion of p18Ink4c (p18), an inhibitor of CDK4 and CDK6, functionally inactivates the RB pathway, stimulates mammary luminal stem cell proliferation, and leads to spontaneous luminal tumor development whereas germline mutation of Brca1 alters the fate of luminal cells and causes luminal-to-basal mammary tumor transformation. We report here that disruption of Brca1 by both germline and epithelium-specific mutation of Brca1 in p18 deficient mice activates epithelial-to-mesenchymal transition (EMT) and induces basal-like breast tumors. Introduction of BRCA1 suppresses expression of EMT-inducing transcription factors (EMT-TFs) and inhibits EMT in mammary tumor cells. Knockdown of BRCA1 in human luminal cancer cells activates EMT and increases tumor formation potential. Consistently, EMT features are inversely correlated with BRCA1 in human breast cancers. These findings provide genetic evidence suggesting that BRCA1 suppresses EMT and inhibits basal-like tumor development. Citation Format: Xin-Hai Pei, Feng Bai, Ho Lam Chan, Alexandria Scott, Matthew D Smith, Cheng Fan, Jason I Herschkowitz, Charles M Perou, Alan S Livingstone, David J Robbins, Anthony J Capobianco. Genetic analysis of the role of Brca1 in suppression of basal-like breast cancer [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P4-05-01.
Histological study and analysis of vascular calcifications in peritoneal biopsies: Adipocytes as new players in encapsulating peritoneal sclerosis?
Authors: Agnieszka Pozdzik, Raja T Nas'r, Monika Tooulou, Pieter Demetter, Anwar Hamade, M. Daudon, Dominique Bazin, Joëlle Nortier
Journal: Journal of the American Society of Nephrology (2014)
Abstract 14478: Impact of Left Ventricular Systolic Function on Clinical Outcomes following Transcatheter Aortic Valve Implantation for Severe Aortic Stenosis
Authors: See Hooi Ewe, Nina A Marsan, Mauro Pepi, Victoria Delgado, Gloria Tamborini, Manuela Muratori, Arnold C.T. Ng, Frank van der Kley, Arend de Weger, Melissa Fusari, Paolo Biglioli, Jeroen J Bax
Journal: Circulation (2010)

Introduction: Left ventricular (LV) systolic dysfunction is a well-known negative prognostic marker in patients with severe aortic stenosis (AS). We examined the effect of baseline LV ejection frac...
Abstract 128: The Effect of Dihydrocapsaicin to Induce Mild Hypothermia in Anesthetized Pigs
Authors: Sung Phil Chung, Jeonghyun Park, Yinlun Weng, Keld Fosgerau, Xiaobo Wu, Shijie Sun, Max Harry Weil, Wanchun Tang
Journal: Circulation (2010)

Introduction: Therapeutic hypothermia is one of the standard treatments in post resuscitation care. The dihydrocapsaicin (DHC) is known to induce hypothermia in a rat cardiac arrest model. However, this effect has not yet been tested in pig model. We assessed the hypothesis that DHC could induce hypothermia in the anesthetized swine model. Methods: Male swine weighting 19.1±1.6 kg were randomly assigned between control and DHC group under anesthesia with pentobarbital. The control group (n=2) received intravenous saline at a rate of 100 ml/hr for 5 hours while the DHC group (n=2) received 2.5 mg/kg/h of DHC (1 mg/ml) in the same manner. The heart rate, blood pressure, and rectal temperature were recorded continuously during infusion. The average ambient room temperature was maintained at 23.5°C and the surface temperature of the animal was maintained at 33.0±0.5°C with a heating lamp. Data were analyzed using the Mann-Whitney test. Results: The baseline temperature was 37.4±0.6°C and was not different bet...
Abstract A39: The activation of β1-integrin by type i collagen coupling with the Hedgehog pathway promotes the epithelial-mesenchymal transition in pancreatic cancer cells
Authors: Wanxing Duan, Qingyong Ma, Jiguang Ma, Qinhong Xu, Jianjun Lei, Erxi Wu
Journal: Cancer Research (2015)

Abstract Pancreatic ductal adenocarcinoma (PDAC), one of the most lethal gastrointestinal cancers, is characterized by the excessive deposition of extracellular matrix (ECM) that has been thought to contribute to the malignant behaviour. However, the detailed mechanism and the contribution of excessive deposition of ECM in PDAC progression remain unclear. A better understanding of the mechanism involved in this process is essential for the design of new effective therapies. In this study, we demonstrated that pancreatic cancer cells exhibited increased proliferation and decreased apoptosis in response to type I collagen. In addition, exposed to type I collagen, PDAC cells lost the expression of E-cadherin and increased expression of mesenchymal markers, including N-cadherin and vimentin, which was correlated with enhanced cell migration and invasiveness. Conversely, the knockdown of β1-integrin abolished the effects induced by type I collagen. Further investigation revealed that type I collagen activates β1-integrin accompanied with significant up-regulation of Gli-1. siRNA specific to Gli-1 reversed the effects of type I collagen on PDAC invasion and epithelial-mesenchymal transition (EMT). These results suggest that there is cross-talk between the β1-integrin signaling pathway and the Hedgehog (HH) pathway in pancreatic cancer and the abnormal activation of the HH pathway plays a key role in the type I collagen-induced effects on pancreatic cancer. Therefore, our findings may have potential significance for the development of new therapeutic strategies to treat this highly aggressive malignancy. Citation Format: Wanxing Duan, Qingyong Ma, Jiguang Ma, Qinhong Xu, Jianjun Lei, Erxi Wu. The activation of β1-integrin by type i collagen coupling with the Hedgehog pathway promotes the epithelial-mesenchymal transition in pancreatic cancer cells. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr A39.
LEPROSY IN MINNESOTA.
Authors: H M Bracken
Journal: JAMA (1899)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Abstract 1544: Early Statin Therapy Reduces Risk Of ICD Shocks In Patients With An Implantable Cardioverter-defibrillator Undergoing Ablation For Ventricular Tachycardia
Authors: T. J Bunch, Paul A Friedman, Bernard J Gersh, Samuel J Asirvatham, Peter A Brady, Yong-Mei Cha, Arshad Jahangir, Stephen C Hammill, Kristi Monahan, Thomas M Munger, Robert F Rea, Win K Shen, Niloufar Tabatabaei, Douglas L Packer
Journal: Circulation (2007)

Background : Lipid lowering therapy reduces mortality in patients with both ischemic and nonischemic cardiomyopathies and recently has been shown to decrease ICD shocks. Radiofrequency ablation (RFA) of recurrent VT in patients with an ICD also reduces shocks following intervention. It is unclear if statin therapy after VT RFA will further impact ICD shock rates. Methods : All patients from 1993–2005 who underwent a RFA procedure for recurrent VT at the Mayo Clinic with an ICD were included. Patient records were extracted for medical and procedural details and all ICD interrogations were reviewed for VT recurrence and therapies. Results: 63 patients (age 62±15 years) were followed over 3.9±3.6 years. Comorbid diseases included: coronary artery disease 37(58%, 34 prior myocardial infarction), ARVD/C 6(10%), nonischemic dilated cardiomyopathy 7(11%), moderate-severe valve disease 14(22%), hypertension 34(54%), and hyperlipidemia 35(56%). Ejection fraction was &lt;0.35 in 34(56%). VT was induced in all patients (LV 55 (LVOT 1), RV 8 (RVOT 3) with multiple inducible VTs in 21(33%). VT was noninducible after RFA in 39(62%) patients. Dismissal medications included: statins 19(30%), beta blockers 40(66%), ACE/ARB 37(61%), diuretics 34(55%), and digoxin 23(37%). 5-year overall survival was 63%(95% CI 55–71). Age, diabetes, and renal insufficiency were associated with increased post ablation mortality, with no medication improving survival. 5-year survival free of ICD shocks was 31%(95% CI 24–38). Only statin therapy at discharge was associated with a decreased risk of ICD shocks [5(26%) versus 26(59%), p=0.020]. 7 additional patients received statins during follow-up, but not at discharge, of these 5(71%) had shocks. Conclusion : Statin use at discharge in patients with an ICD undergoing RFA for refractory VT significantly reduced recurrent ventricular arrhythmias and ICD shocks. Although the mechanism underlying the effects of statins on arrhythmic recurrence early after RFA requires further study, these data support aggressive therapy of the underlying substrate responsible for the VT.