tbuckley/cabot-search huggingface dataset:
Abstract 17339: Blood Oxygenation Level Dependent Magnetic Resonance Imaging: a Tool for Objective Assessment of Perfusion in the Lower Limb
Authors: Adnan Bajwa, Roman Wesolowski, Ashish S Patel, Prakash Saha, Francesca Ludwinski, Alberto Smith, Eike Nagel, Bijan Modarai
Journal: Circulation (2014)

Aims: No objective method exists for measuring muscle perfusion in the lower leg. We aimed to determine the utility of blood oxygenation level dependent (BOLD) MRI for assessment of lower limb perfusion.

Methods: BOLD MRI was performed on the calf of patients with critical limb ischaemia (CLI, before and after successful revascularisation), age-matched controls, and healthy volunteers, using a 3T magnet (Fig 1a). A thigh cuff was inflated to suprasystolic pressure for 5mins then released to provoke reactive hyperaemia. Time to peak (TTP), the rate of increase in signal after decuffing (gradient) and time to half ischaemia (1/2T) were used to measure relative differences in signal intensity for each muscle group (Fig1b).

Results: A longer TTP, lower gradient and shorter 1/2T (ANOVA, P<0.001 for all) was measured in the ischaemic leg of CLI patients (n=21) compared with the patient’s contralateral (control) limb (n=21), the limbs of age-matched controls (n=4) and the limbs of healthy volunteers (n=9) in each muscle group (Fig 1c). BOLD MRI was carried out after limb revascularisation (n=5, pre ABPI 0.45 vs. post ABPI 0.79). At 1-7 days post intervention imaging revealed significantly shorter TTP (89.7±5.4s vs. 141.7±7.1s), higher gradient (6.19±0.56 vs. 2.61±0.36) and longer 1/2T (201.6±5.8s vs. 173.5±7.7s) compared with pre intervention values respectively (paired t-test, P<0.001 for all, Fig 1d). In all cases, the soleus and anterior muscle groups discriminated best between ischaemic and control limb perfusion.

Conclusions: BOLD MRI can reliably discriminate between well and poorly perfused limbs. Evaluating changes in BOLD signal may better guide lower limb intervention and provide an objective means of quantifying improvements immediately after treatment, which may ultimately lead to improved limb salvage.

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Localization of Gene Action in the Causation of Lung and Mammary Gland Tumors in Mice&lt;xref ref-type="fn" rid="fn1"&gt;1&lt;/xref&gt;
Authors: Heston We
Journal: JNCI Journal of the National Cancer Institute (1954)

Localization of Gene Action in the Causation of Lung and Mammary Gland Tumors in Mice Get access W. E. Heston W. E. Heston National Cancer Institute,2Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 15, Issue 3, December 1954, Pages 775–789, https://doi.org/10.1093/jnci/15.3.775 Published: 01 December 1954
What Now, Mad Cow?
Authors: Tracy Hampton
Journal: JAMA (2004)

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
Anti‐IL‐33 antibody has a therapeutic effect in a murine model of allergic rhinitis
Authors: Y. H. Kim, T. Y. Yang, C.‐S. Park, S.‐H. Ahn, B. K. Son, J. H. Kim, D. H. Lim, T. Y. Jang
Journal: Allergy (2011)

Interleukin (IL)-33 is involved in the Th2 immune response and could play an essential role in nasal allergy. Therefore, we aimed to investigate the therapeutic potential of anti-IL-33 for allergic rhinitis (AR).Twenty-four BALB/c mice were used. In group A (control group, n = 6), mice were sensitized and challenged with saline. Group B [ovalbumin (OVA) group, n = 6] mice received intraperitoneal and intranasal OVA challenge. In group C (control IgG group, n = 6), mice were injected intraperitoneally with rabbit control IgG before OVA challenge. In group D (anti-IL-33 group, n = 6), anti-IL-33 was injected before challenge. We evaluated the number of nose-scratching events and external morphology; serum total and OVA-specific IgE; number of eosinophils, neutrophils, and lymphocytes in bronchoalveolar lavage (BAL) fluid; histopathologic examination of nasal cavity; and IL-4, IL-5, and IL-13 in BAL fluid.Anti-IL-33 treatment significantly reduced the nose-scratching events and ameliorated skin denudation. Serum total and OVA-specific IgE was significantly decreased in group D. The number of eosinophils in BAL fluid was also significantly decreased. Eosinophilic infiltration in the nasal cavity was significantly decreased in group D. IL-4, IL-5, and IL-13 in BAL fluid were also significantly decreased after treatment.Anti-IL-33 antibody has a therapeutic potential for experimental AR.
Abstract 19839: Clinical and Economic Burden of Rheumatic Heart Disease in Low-Income Nations: Estimating the Cost-of-Illness in India and Uganda
Authors: Alexander T Sandhu, Kathikeyan G, Ann Bolger, Emmy Okello, Dhruv S Kazi
Journal: Circulation (2014)

Introduction: Rheumatic heart disease (RHD) strikes young adults at their peak economic productivity. Defining the global economic burden of RHD may motivate investments in research and prevention, yet prior approaches considering only medical costs may have underestimated the cost of illness. Objectives: To estimate the clinical and economic burden of RHD in India and Uganda. Outcomes were disability-adjusted life years (DALYs), direct medical costs, and indirect costs due to disability and premature mortality (2012 USD). Methods: We used a discrete-state Markov model to simulate the natural history of RHD using country-, age-, and gender-specific estimates from the literature and census data. We estimated direct medical costs from WHO-CHOICE and Disease Control and Prevention 3 publications. We conservatively estimated indirect costs (lost earnings and imputed caregiver costs) from World Bank data using novel economic methods. Results: In 2012, RHD generated 6.1 million DALYs in India and cost USD 10.7 billion (Table 1), including 1.8 billion in direct medical costs and 8.9 billion in indirect costs. During the same period, RHD produced 216,000 DALYs in Uganda, and cost USD 414 million, and, as in India, indirect costs represented the majority (88%) of the cost of illness. In both countries, women accounted for the majority (71-80%) of the DALYs; in Uganda, women bore 75% of the total cost. In sensitivity analyses, higher progression rates for subclinical disease doubled direct costs and DALYs. Conclusion: RHD exacts an enormous toll on the populations of India and Uganda, and its economic burden may be grossly underestimated if indirect costs are not systematically included. Women bear a disproportionate clinical burden from pregnancy-related complications. These results suggest that effective prevention and screening of RHD may represent a sound public health investment, particularly if targeted at high-risk subgroups such as young women.
Treatment of Dry Eye Syndrome with Orally Administered CF101
Authors: Isaac Avni, Hanna J. Garzozi, Irina S. Barequet, Fanni Segev, David Varssano, Gil Sartani, Noa Chetrit, Erez Bakshi, David Zadok, Oren Tomkins, Gilad Litvin, Kenneth A. Jacobson, Sari Fishman, Zivit Harpaz, Motti Farbstein, Sara Bar Yehuda, Michael H. Silverman, William D. Kerns, David R. Bristol, Ilan Cohn, Pnina Fishman
Journal: Ophthalmology (2010)
Abstract 250: Effects of Mild Hypothermia on Cerebral Lactate Metabolism in a Rat Model of Cardiac Arrest
Authors: Jiangang Wang, Ping Gong, Shen Zhao, Jie Qian, Zhengfei Yang, Xiaobo Wu, Jena Cahoon, Neil Duggal, Wanchun Tang
Journal: Circulation (2014)

Introduction: A strong relationship between lactate clearance rate and better outcomes in patients of cardiac arrest (CA) has been demonstrated. Mild hypothermia improves neurological outcomes and survival after CA. In the present study, we investigated the effect of mild hypothermia on cerebral lactate metabolism in a rat model of CA. Hypothesis: Mild hypothermia accelerates cerebral lactate clearance rate in a rat model of CA. Methods: Ten male Sprague-Dawley rats were randomized into two groups: hypothermic (HT, n=5) and normothermic (NT, n=5) groups. After 8 mins of untreated ventricular fibrillation, precordial compression and mechanical ventilations were initiated for 8 mins. The core temperature was decreased to 33±0.5°C after 14 mins of resuscitation with a combination of ice packs, an electrical fan and a cooling blanket. The temperature was maintained at 33°C for 8 hrs. The jugular vein lactate concentration was measured at baseline (BL), 2, 4 and 8 hrs after resuscitation (PR 2, 4 and 8 hrs). R...
Genetic Variants at Chromosome 9p21 and Risk of First Versus Subsequent Coronary Heart Disease Events
Authors: Riyaz S. Patel, Folkert W. Asselbergs, Arshed A. Quyyumi, Tom M. Palmer, Chris I. Finan, Vinicius Tragante, John Deanfield, Harry Hemingway, Aroon D. Hingorani, Michael V. Holmes
Journal: Journal of the American College of Cardiology (2014)

The purpose of this analysis was to compare the association between variants at the chromosome 9p21 locus (Ch9p21) and risk of first versus subsequent coronary heart disease (CHD) events through systematic review and meta-analysis. Ch9p21 is a recognized risk factor for a first CHD event. However, its association with risk of subsequent events in patients with established CHD is less clear. We searched PubMed and EMBASE for prospective studies reporting association of Ch9p21 with incident CHD events and extracted information on cohort type (individuals without prior CHD or individuals with established CHD) and effect estimates for risk of events. We identified 31 cohorts reporting on 193,372 individuals. Among the 16 cohorts of individuals without prior CHD (n = 168,209), there were 15,664 first CHD events. Ch9p21 was associated with a pooled hazard ratio (HR) of a first event of 1.19 (95% confidence interval: 1.17 to 1.22) per risk allele. In individuals with established CHD (n = 25,163), there were 4,436 subsequent events providing >99% and 91% power to detect a per-allele HR of 1.19 or 1.10, respectively. The pooled HR for subsequent events was 1.01 (95% confidence interval: 0.97 to 1.06) per risk allele. There was strong evidence of heterogeneity between the effect estimates for first and subsequent events (p value for heterogeneity = 5.6 × 10−11). We found no evidence for biases to account for these findings. Ch9p21 shows differential association with risk of first versus subsequent CHD events. This has implications for genetic risk prediction in patients with established CHD and for mechanistic understanding of how Ch9p21 influences risk of CHD.
Analysis of Vλ-Jλ expression in plasma cells from primary (AL) amyloidosis and normal bone marrow identifies 3r(λIII) as a new amyloid-associated germline gene segment
Authors: Vittorio Perfetti, Simona Casarini, Giovanni Palladini, Maurizio Colli Vignarelli, Catherine Klersy, Marta Diegoli, Edoardo Ascari, Giampaolo Merlini
Journal: Blood (2002)
Decreased BRCA1 protein expression alert the response of MCF7 cells to tamoxifen
Authors: Zhijiu Zhong, Alimatou Minkeu, Judy Quong, Andrew Quong
Journal: Clinical Cancer Research (2008)

B44   Approximately 60% of breast cancers are estrogen receptor-positive and tamoxifen, which targets the estrogen receptor (ER), is one of the most effective treatments. However, de novo and acquired tamoxifen resistance remain important clinical problems. The circumvention of tamoxifen resistance using rational therapeutic approaches requires an understanding of the underlying molecular mechanisms of the cellular response to tamoxifen. Decreased protein expression of the tumor suppressor BRCA1 has been observed in sporadic breast cancer and is associated with poor prognosis and a more aggressive phenotype. BRCA1 has also been shown to directly inhibit ER activity. ER activity plays a major role in mammary epithelial cell proliferation during carcinogenesis so it is not surprising that decreased BRCA1 protein is associated with poor prognosis. Furthermore, tamoxifen was shown to promote mammary cancer development in a mouse model of BRCA1-mutation-related breast cancer. In order to reveal the relationship between decreased BRCA1 protein levels and tamoxifen response, MCF7 cells stably expressing shRNA targeted against the BRCA1 gene were established using recombinant retrovirus, resulting in a 38% reduction of BRCA1 protein levels compared to cells expressing scrambled control shRNA. BRCA1 knockdown was accompanied by increased cell proliferation and decreased response to tamoxifen as determined by MTT assay. To asses the molecular mechanisms of these effects, we used mass spectrometry to determine the global changes in protein expression. For these studies, iTRAQ isobaric tags were used the peptides were separated with two-dimensional liquid chromatography. Tandem mass spectrometry was performed on an ABI 4800 MALDI ToF/ToF. Changes in levels of expression of proteins involved in processes such as metabolism, differentiation, cell death and biosynthesis were identified. An understanding of the mechanisms of tamoxifen resistance is the first step toward developing new therapeutic strategies for women with this phenotype. Identification of global protein expression patterns will provide valuable information toward understanding the mechanisms underlying tamoxifen response and can be used immediately to develop a clinical strategy for treating tamoxifen resistant tumors. A greater understanding of the cellular and molecular mechanisms of tamoxifen will lead to individualized treatment against breast cancer.
Abstract 17063: Enhanced Prediction of Heart Failure 30-Day Readmission Risk With Four Readily-Available Clinical Variables
Authors: Nicholas Wettersten, Machelle Wilson, Kathleen Tong, Javier E López
Journal: Circulation (2014)

Introduction: Heart failure (HF) readmissions, with ~25% within 30 days of discharge, can be reduced with costly post-hospitalization interventions. Determining which patients will benefit from these interventions remains a critical challenge. Hypothesis: We aimed to devise a simple model to predict 30-day HF readmission risk. Methods: Patients ≥21 years of age admitted for HF to a single academic center from July 1st, 2008 to December 31st, 2009 were identified by billing codes for HF. Patients were excluded if they died within 90 days, were transferred, discharged to hospice or prison, or later admitted electively or for a surgical emergency not related to HF. Demographics, co-morbidities, laboratories, vitals, and discharge medications (27 variables) were tested as predictors for risk of 30 day readmission. First, independent univariate testing of categorical variables was performed utilizing a retention p-value of &lt; 0.2. Next, continuous variables and retained categorical variables were tested in a multivariable model with retention of variables with p-value &lt; 0.1. False discovery rate was controlled by the method of Benjamini and Hochberg. Statistical analyses were performed using SAS® software version 9.3. Results: Of 1253 HF admissions, 657 (55.8% men, age 60.9 ± 13.8 men, 66.8 ± 14.5 women) met criteria with complete data. Twenty percent were readmitted within 30 days. Odds for readmission increased 1.6% for every 100 pg/ml increase in BNP (p=0.082), 5.6% for each additional discharge medication (p=0.003), 200% if not discharged on an ACE-I/ARB (p=0.001), and 7% for every 10 mmHg increase in systolic blood pressure at discharge compared to admission (p=0.078). Conclusion: One laboratory value and 3 clinical variables were predictive of 30-day HF readmission risk in a multivariate prediction model. The 3 clinical predictors provoke the idea that “in hospital” care is a predictor and potential target for intervention to reduce 30-day readmission risk. Future validation studies should help define standard-of-care interventions that could still be improved to reduce readmission rates in HF patients as well as address the relative cost of more intense hospital interventions over outpatient interventions.
Abstract P4-04-26: Down-regulation of p16INK4a inhibits miR-146b-5p and modulates IL-6 in breast stromal fibroblasts
Authors: Mysoon M Al-Ansari, Abdelilah Aboussekhra
Journal: Cancer Research (2015)

Abstract Breast cancer is a major health problem that threatens millions of women’s lives each year worldwide. Cancer-associated fibroblasts (CAFs), which constitute the major component of the tumor stroma, have been reported to actively contribute to tumor cells proliferation and invasion. Recently, we have shown down-regulation of the tumor suppressor p16INK4a protein in breast cancer-associated fibroblasts. Moreover, p16INK4a deficiency led to the activation of the stromal fibroblasts, which express/secrete elevated levels of IL-6, a major player in breast carcinogenesis. We have shown here that p16INK4a negatively regulates the IL-6 expression and secretion in breast stromal fibroblasts. Furthermore, we have shown that IL-6 is playing a major role in mediating the paracrine pro-carcinogenic effect of p16-deficient fibroblasts. We have also shown that p16INK4a inhibits the IL-6 expression in a miRNA-146b-5p-dependent manner. Importantly, we present clear evidence that miR-146b-5p inhibition activates breast stromal fibroblast. Indeed, miR-146b-5p inhibition increased the migration/invasion abilities of breast stromal fibroblasts, and the paracrine effect of these cells on the migration/invasion of breast cancer cells. Furthermore, miR-146b-5p-deficient stromal fibroblasts triggered epithelial to mesenchymal transition in breast cancer cells in a paracrine manner. In addition, we have shown that miR-146b-5p is down-regulated in CAFs as compared to their adjacent counterpart fibroblasts. These results indicate that p16INK4a negatively regulates IL-6 through the activation of miR-146b-5p, which plays a major role in repressing breast stromal fibroblasts and inhibiting their pro-carcinogenic effects. This indicates that miR-146b-5p has cell-non-autonomous tumor suppressor function. Therefore, this miRNA could be of great therapeutic value. Citation Format: Mysoon M Al-Ansari, Abdelilah Aboussekhra. Down-regulation of p16INK4a inhibits miR-146b-5p and modulates IL-6 in breast stromal fibroblasts [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 P4-04-26.
Rise and Development of Liquefaction of Gases.
Authors: Willett Lepley Hardin
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 1515: Outcomes of Patients With Acute Coronary Syndromes and Prior Coronary Artery Bypass Grafting. Results From the Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT-TIMI 22) and the Aggrastat to Zocor (A to Z) trials.
Authors: Emmanouil S Brilakis, James A de Lemos, Christopher P Cannon, Stephen D Wiviott, Sabina A Murphy, David A Morrow, Marc S Sabatine, Subhash Banerjee, Michael A Blazing, Robert M Califf, Eugene Braunwald
Journal: Circulation (2007)

Background: Patients with prior coronary artery bypass graft surgery (CABG) who develop acute coronary syndromes (ACS) are at high risk for major adverse cardiac events. The benefits of intensive statin therapy, targeting an LDL cholesterol of &lt; 70 mg/dL, in patients with ACS and prior CABG have not been well studied. Methods: The effect of intensive vs. moderate statin therapy was assessed in patients with and without prior CABG participating in the Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT TIMI 22) or the Aggrastat to Zocor (A to Z) trials. Results: Six hundred and forty of the 8655 patients (7.4%) enrolled in PROVE IT-TIMI 22 or A to Z had undergone CABG prior to enrollment. Prior CABG patients were older, more likely to be men and had a higher TIMI risk score. After a median follow-up of 2 years, compared to patients without prior CABG, those with prior CABG had higher risk of cardiovascular death (6.2 vs. 2.8%), myocardial infarction (14.2% vs. 6.6%), and readmission for ACS (7.9% vs. 4.4%) (p&lt;0.001 for all comparisons), but a lower rate of repeat coronary revascularization (22.7% vs. 26.9%, p=0.01). Compared to moderate statin therapy, intensive statin therapy decreased the combined endpoint of cardiovascular death, myocardial infarction, stoke, and readmission for an acute coronary syndrome (A to Z primary endpoint) to a similar extent in patients with and without prior CABG (Table ). The benefit of intensive statin therapy in prior CABG patients appeared to be due to a reduction in unstable angina requiring hospitalization, with no significant difference in the incidence of death, myocardial infarction, or coronary revascularization. Conclusions: Compared to ACS patients without prior CABG, those with prior CABG have significantly higher risk for death and adverse cardiac events and appear to show similar benefit from intensive statin therapy. Effect of intensive statin therapy on outcomes of patients with and without prior CABG