tbuckley/cabot-search huggingface dataset:
Angiotensin(1–7) attenuates the progression of streptozotocin-induced diabetic renal injury better than angiotensin receptor blockade
Authors: Kai Zhang, Xiao Meng, Dongmei Li, Jianmin Yang, Jing Kong, Panpan Hao, Tao Guo, Meng Zhang, Yun Zhang, Cheng Zhang
Journal: Kidney International (2014)

To explore the potential therapeutic effects of angiotensin(1-7) (Ang(1-7)), an endogenous ligand of the Mas receptor, on streptozotocin-induced diabetic nephropathy, male Wistar rats were randomly divided into two groups: a control group and a diabetic model group. After 12 weeks, the diabetic rats were divided into subgroups for 4-week treatments consisting of no-treatment group, small-, moderate-, and large-dose Ang(1-7) groups, a valsartan group, a large-dose Ang(1-7) plus valsartan group, and an A779 (antagonist of the Mas receptor) group, each with 15 rats. Ang(1-7) improved renal function, attenuated glomeruli sclerosis, oxidative stress, and cell proliferation, decreased the expression of collagen IV, TGF-β1, VEGF, NOX4, p47phox, PKCα, and PKCβ1, and the phosphorylation of Smad3. In the rat mesangial HBZY-1 cell line, Ang(1-7) decreased high-glucose-induced oxidative stress, the proliferation and expression of NOX4, p47phox, and TGF-β1, the phosphorylation of Smad3, collagen IV, and VEGF, and the membrane translocation of PKCα and PKCβ1. A779 blocked the effects of Ang(1-7) both in vivo and in vitro. The effects of large-dose Ang(1-7) alone and in combination with valsartan were superior to valsartan alone, but the combination had no significant synergistic effect compared with Ang(1-7) alone. Thus, Ang(1-7) ameliorated streptozotocin-induced diabetic renal injury. Large-dose treatment was superior to valsartan in reducing oxidative stress and inhibiting TGFβ1/Smad3- and VEGF-mediated pathways.
753-2 Biplane and Multiplane Transesophageal Echocardiography in Suspected Acute Aortic Dissection
Authors: Andre Keren, Charles B. Kim, Bob Hu, Irina Eyngorina, Margaret E. Billingham, R. Scott Mitchell, D. Craig Miller, Richard L. Popp, Ingela Schnittger
Journal: Journal of the American College of Cardiology (1995)
A CASE OF DOUBLE PLEURISY WITH EFFUSION.
Authors: J. F. McGARRAHAN
Journal: JAMA (1907)

Cases of double pleurisy with effusion are seemingly rare enough to warrant the following report: <h3>Patient.</h3> —M. W., aged 11½, was first seen June 18, 1903. <h3>Family History.</h3> —On the father's side this was negative. There had been several cases of pulmonary tuberculosis among the mother's sisters, one of whom was ailing at the time this child was seen. A sister of the patient had pleurisy with effusion four years before, which required early aspiration and the girl made a good recovery. One brother died at 4 years of diphtheria. <h3>Personal History.</h3> —The girl had typhoid fever at the age of 8. Six months before the present attack she developed a rash resembling scarlet fever, which disappeared in 24 hours. The child was not very sick at the time. Ten days before I was called she came home from school with fever, headache, vomiting and nosebleed. A harsh dry cough
Interleukin 2 Therapy for Disseminated Cancer
Authors: Tom Smith
Journal: JAMA (1987)

<h3>To the Editor.—</h3> Lotze et al<sup>1</sup>report that interleukin 2 (IL-2) can produce objective regressions in patients with melanoma. I am concerned that other factors in the treatment protocol rather than IL-2 may be responsible for some of the antitumor activity. All patients received ranitidine hydrochloride or cimetidine hydrochloride to reduce histamine-related side effects and prevent gastritis. Histamine type 2 receptor antagonists such as ranitidine or cimetidine inhibit activation of suppressor T cells<sup>2</sup>and may allow cytotoxic T cells to more effectively kill cancer cells.<sup>3</sup>I recently found complete regression of all melanoma nodules in a patient treated with ranitidine (unpublished data), and other researchers have noted remissions in patients treated with cimetidine. Responding tumors have included mycosis fungoides,<sup>4</sup>solid tumors,<sup>5</sup>and melanoma.<sup>6</sup>Preliminary work using cimetidine plus coumarin<sup>7</sup>showed three of eight patients with melanoma responding, in a way that does not
Aborted Suicide Attempts: A New Classification of Suicidal Behavior
Authors: Mary E. Barber, Peter M. Marzuk, Andrew C. Leon, Laura Portera
Journal: American Journal of Psychiatry (1998)

OBJECTIVE: With the goal of ultimately finding early suicide predictors, the authors undertook a study of aborted suicide attempts. They defined such an attempt as an event in which an individual comes close to attempting suicide but does not complete the act and thus sustains no injury. METHOD: The authors interviewed a random sample of 135 adult psychiatric inpatients concerning their past suicidal behavior. Using standardized scales, they assessed suicidal intent for aborted suicide attempts and actual suicide attempts, as well as degree of injury for actual attempts. RESULTS: Over half of the 135 subjects reported making at least one aborted suicide attempt. Aside from younger age, no demographic characteristics were associated with aborted attempts. Aborted attempts were reported more often in subjects with a diagnosis of borderline personality disorder than in subjects with other diagnoses. Intent scores for aborted attempts were comparable to those for actual suicide attempts. Subjects who had made an aborted attempt were nearly twice as likely to have made an actual suicide attempt as subjects with no aborted attempts. Among subjects with both aborted and actual attempts, the first aborted attempt preceded the first actual attempt approximately half the time. CONCLUSIONS: Aborted suicide attempts were reported commonly by psychiatric inpatients, had a similar level of intent as actual attempts, and were highly associated with actual attempts. Thus, clinicians should specifically ask patients about aborted attempts as a part of the suicide history. Further study is needed to examine the association between aborted suicide attempts and suicide.
Natural evolution of skin‐test sensitivity in patients with IgE‐mediated hypersensitivity to cephalosporins
Authors: A. Romano, F. Gaeta, R. L. Valluzzi, A. Zaffiro, C. Caruso, D. Quaratino
Journal: Allergy (2014)

Abstract There are studies demonstrating that skin‐test sensitivity to penicillins can decrease over time and that allergic patients may lose sensitivity if the responsible compounds are avoided. With regard to subjects with I gE‐mediated hypersensitivity to cephalosporins, however, such studies are lacking. We evaluated prospectively in a 5‐year follow‐up 72 cephalosporin‐allergic patients. After the first evaluation, patients were classified into two groups according to their patterns of allergologic‐test positivity: to both penicillins and cephalosporins (group A), or only to cephalosporins (group B). Skin tests and serum‐specific IgE assays were repeated 1 year later and, in case of persistent positivity, 3 and 5 years after the first allergologic examination. Seven (43.7%) of the 16 subjects of group A and 38 (67.8%) of the 56 patients of group B became negative; one was lost to follow‐up. Patients of group B became negative sooner and more frequently than group A subjects.
Accelerating the clearance of mutant huntingtin protein aggregates through autophagy induction by europium hydroxide nanorods
Authors: Peng-Fei Wei, Li Zhang, Susheel Kumar Nethi, Ayan Kumar Barui, Jun Lin, Wei Zhou, Yi Shen, Na Man, Yun-Jiao Zhang, Jing Xu, Chitta Ranjan Patra, Long-Ping Wen
Journal: Biomaterials (2013)
A5.20 Intravenous Immunoglobulin Induces Functionnal Silencing in Human B Lymphocytes
Authors: Sophie Hillion, Jean-François Seité, Carole Goutsmedt, Pierre Youinou, Jacques-Olivier Pers
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Purpose/Objective</h3> Inappropriate B cell receptor (BCR) signalling contributes to the activation of auto-antibody-producing B cells in many autoimmune diseases. These diseases results from a break in B-cell tolerance which is normally maintained by the mechanisms of anergy, receptor editing and deletion. We previously showed that IVIg modulates many B cell responses through a sialic acid-CD22 lectin interaction (Séité, <i>Blood</i> 2010, Séité, <i>J Autoimmunity</i>, 2011). Here, we reasoned that IVIg could modulate B-cell fate and may render autoreactive B cells tolerant through induction of a functional unresponsiveness response to BCR stimulation. <h3>Material and Methods</h3> Tonsilar B-cells were stimulated in the presence of different fractions of IVIg. We analysed subsequent responses to BCR stimulation by confocal microscopy, quantitative RT-PCR, FACS and Western-blot analysis. <h3>Results</h3> First, we observed that up-regulation of costimulatory molecules CD86, CD80 and CD40 induced by BCR cross-linking was down-regulated after IVIg incubation and was associated with a massive reduction of tyrosine phosphorylation. Low mobilisation of intracellular Calcium, which is a hallmark of anergy, was also observed in IVIg-treated B cells. Next, we observed that following BCR stimulation, IVIg blocks BCR aggregation within lipid rafts and increases its internalisation. Consequently, BCR stimulation is not achievable and results in a low activation of the PI3K-Akt signalling pathway. Finally, we demonstrated that IVIg down-regulates NFκB activation and promotes NFAT transcription factors entry in the nucleus. These findings demonstrated that IVIg induces a selective transcriptional programme, allowing nuclear signals to be independently activated, leading to alternative B cell fates. <h3>Conclusions</h3> Our data suggest that IVIg could induce B cells to adopt a state that results in a functional silencing, also called anergy. Our findings provide insights into the effectiveness of IVIg in treating pathologies associated with the loss of B cell tolerance. We also describe a new model to explore the complexity of positive versus negative selection in human B cells.
Heart Rate Recovery and Impact of Myocardial Revascularization on Long-Term Mortality
Authors: Michael S. Chen, Eugene H. Blackstone, Claire E. Pothier, Michael S. Lauer
Journal: Circulation (2004)

Background— Although heart rate recovery (HRR) predicts mortality after exercise testing, its ability to identify patients likely to benefit after revascularization is unknown. We sought to determine whether HRR can identify patients likely to have improved survival after revascularization. Methods and Results— A total of 8861 patients undergoing treadmill nuclear or echocardiographic testing were divided into early revascularization (percutaneous coronary intervention or bypass surgery within 3 months) and non–early revascularization groups. Prespecified subgroup analysis was performed based on the presence or absence of ischemia, normal or impaired functional capacity, and normal or abnormal HRR. The primary end point was all-cause mortality. Early revascularization occurred in 552 patients. We propensity-matched 508 early revascularization patients to 508 non–early revascularization patients on the basis of 48 possible confounders. This constituted the present study cohort. During 8-year follow-up, 232 patients died. Overall, revascularization was associated with a slight but not significant decrease in mortality (hazard ratio [HR] 0.80, 95% CI 0.62 to 1.03). A significant decrease in mortality after revascularization was present in patients with imaging evidence of stress-induced ischemia (HR 0.62, 95% CI 0.44 to 0.87). Ischemic patients with normal HRR had significantly lower mortality with revascularization (HR 0.55, 95% CI 0.34 to 0.90), whereas ischemic patients with abnormal HRR did not (HR 0.78, 95% CI 0.47 to 1.29); however, the test for interaction between these 2 groups was not significant ( P =0.34). Conclusions— In patients with imaging evidence of myocardial ischemia, an abnormal HRR is associated with a nonsignificant trend toward blunting the survival improvement associated with early revascularization. HRR does not appear to identify patients likely to have a survival benefit.
Isolating patients in hospital to control infection. Part V--An isolation system.
Authors: K D Bagshawe, R Blowers, O M Lidwell
Journal: BMJ (1978)

New Zealand, and this subject has been recently discussed in an editorial,5 where it was noted that, for reasons that are far from clearly expressed, the recent government committee shied away from any no-fault scheme for compensation for medical accidents.I think that failing to do a malaria smear for someone with symptoms who has returned from a malarious area should automatically be considered negligent and result in the offer of compensation if death occurs.
Abstract 5156: Hyperglycemia enhances IGF-I responses and alters the AMPK activation profile that protects against metformin-induced growth inhibition in pancreatic cancer cells
Authors: Emelie Karnevi, Katarzyna Said, Roland Andersson, Ann H. Rosendahl
Journal: Cancer Research (2012)

Abstract Epidemiological studies have shown direct associations between type 2 diabetes (T2D) and obesity, both conditions associated with hyperglycemia and hyperinsulinemia, and the risk of pancreatic cancer. Up to 80% of pancreatic cancer patients are diagnosed with either impaired glucose tolerance or new-onset T2D one or two years prior to their cancer diagnosis. Recent population studies indicate that the incidence of pancreatic cancer is reduced among diabetics taking metformin, an insulin-sensitizing and glucose lowering drug. We investigated the effects of exposure of pancreatic cancer cells to high glucose levels on their growth and response to metformin. We found that metformin significantly reduced the proliferation of pancreatic cancer cells under normal glucose conditions, but that hyperglycemia protected against the metformin-induced growth inhibition. The antiproliferative actions of metformin were associated with an activation of AMP-activated protein kinase AMPK(T172) together with a dose-dependent suppression of the insulin/insulin-like growth factor (IGF) signaling mediators IRS-1 and phosphorylated AKT. Furthermore, exposure to metformin during normal glucose led to increased apoptosis as measured by poly(ADP-ribose) polymerase (PARP) cleavage. In contrast, exposure to high glucose promoted a more robust IGF-I response and AKT activation, that stimulated AMPK(S485) phosphorylation and suppressed AMPK(T172) phosphorylation resulting in reduced antiproliferative and apoptotic effects by metformin. In conclusion, our results indicate that metformin has direct antitumor activities in pancreatic cancer cells involving AMPK(T172) activation and modulation of the insulin/IGF signaling pathways. However, hyperglycemic conditions enhance the insulin/IGF-I responses resulting in an altered AMPK activation profile that prevent metformin from fully switching of the growth promoting signals in pancreatic cancer cells. 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 5156. doi:1538-7445.AM2012-5156
The glomic arteries
Authors: D. Heath, C. Edwards
Journal: Cardiovascular Research (1971)

Journal Article The glomic arteries Get access Donald Heath, Donald Heath From the Department of Pathology, University of Liverpool Search for other works by this author on: Oxford Academic PubMed Google Scholar Christopher Edwards Christopher Edwards From the Department of Pathology, University of Liverpool Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 5, Issue 3, July 1971, Pages 303–312, https://doi.org/10.1093/cvr/5.3.303 Published: 01 July 1971
71. Alpha 1 Antitrypsin (AAT) Gene Therapy for the Prevention of Type 1 Diabetes
Authors: Sihong Song, Yuanqing Lu, Mei Tang, Bin Zhang, Clive Wasserfall, Martha Campbell-Thompson, Mark Atkinson
Journal: Molecular Therapy (2006)

Type 1 diabetes is an autoimmune disease that results in the destruction of insulin producing b cells in the pancreatic islets. Although multiple factors contribute to this disease, an imbalance of the immune regulatory pathways plays an important role in the development of type 1 diabetes. Therefore, immunoregulatory and anti-inflammatory strategies hold great potential for the prevention of this autoimmune disease. Alpha 1 antitrypsin (AAT) is a serine proteinase inhibitor and exhibits various anti-inflammatory effects and protects against tissue damage or injury. In order to test the feasibility of AAT gene therapy for the prevention of type 1 diabetes, we have conducted a serial of experiments using rAAV vectors (serotype 1 and 2) for muscle gene delivery in non-obese diabetes (NOD) mouse model. Results from these studies showed that AAT gene therapy, contrary to control vector (expressing elafin) and saline, decreased insulitis, reduced the levels of autoantibody and prevented type 1 diabetes efficiently and in dose-dependent manner. T cell receptor spectratyping indicated that AAT gene therapy altered T cell repertoire diversity in splenocytes from NOD mice. Adoptive transfer experiments demonstrated that AAT gene therapy attenuated cellular immunity associated with beta cell destruction. Our results also showed that AAT protected islet cells against apoptosis and block cytotoxicity of NK cells. In summary, these data clearly demonstrate that AAT gene therapy efficiently prevented type 1 diabetes development in NOD mice and suggest a potential clinical application of this approach for type 1 diabetes prevention. In addition, that AAT gene therapy attenuates an autoimmune condition supports further investigations for application to other autoimmune disorders.
Sibling Cardiovascular Disease as a Risk Factor for Cardiovascular Disease in Middle-aged Adults
Authors: Joanne M. Murabito
Journal: JAMA (2005)

While parental cardiovascular disease (CVD) doubles the risk for CVD in offspring, the extent of increased risk associated with sibling CVD is unclear.To determine, using validated events, whether sibling CVD predicts outcome in middle-aged adults independent of other risk factors.The Framingham Offspring Study, an inception cohort of the Framingham Heart Study, a prospective population-based cohort study initiated in 1948 with the offspring cohort initiated in 1971. Participants (n = 2475) were members of the offspring cohort aged 30 years or older, free of CVD, and with at least 1 sibling in the study; all were followed up for 8 years.Association of sibling CVD with 8-year personal risk for CVD using pooled logistic regression. A secondary analysis restricted to offspring with both parents in the study assessed the joint impact of parental and sibling CVD occurrence.Among 973 person-examinations in the sibling CVD group (mean age, 57 years) and 4506 person-examinations in the no sibling CVD group (mean age, 47 years), 329 CVD events occurred during follow-up. Baseline risk factors were more prevalent in the sibling CVD group compared with the no sibling CVD group. Sibling CVD was associated with a significantly increased risk for incident CVD (age- and sex-adjusted odds ratio [OR], 1.55; 95% confidence interval [CI], 1.19-2.03). Adjustment for risk factors did not substantially attenuate the risk (adjusted OR, 1.45; 95% CI, 1.10-1.91). In the analysis restricted to persons with both parents in the study, in models adjusting for both sibling and parental CVD, the multivariable-adjusted OR for sibling CVD (1.99; 95% CI, 1.32-3.00) exceeded that for parental CVD (1.45; 95% CI, 1.02-2.05).Using validated events, sibling CVD conferred increased risk of future CVD events above and beyond established risk factors and parental CVD in middle-aged adults.
The ubiquitin ligase gp78 promotes sarcoma metastasis by targeting KAI1 for degradation
Authors: Yien Che Tsai, Arnulfo Mendoza, Jennifer M Mariano, Ming Zhou, Zlatka Kostova, Bo Chen, Timothy Veenstra, Stephen M Hewitt, Lee J Helman, Chand Khanna, Allan M Weissman
Journal: Nature Medicine (2007)
Improved gas exchange after pneumonectomy in an adult with incomplete pulmonary vein atresia.
Authors: T S van der Werf, G P Mannes, J M Hew, R G Grevink, T W van der Mark, T Ebels, G H Koeter
Journal: Thorax (1994)

Atresia of the pulmonary veins of the left lung and the right upper lobe with moderate pulmonary hypertension was diagnosed in a 20 year old man presenting with exertional dyspnoea and haemoptysis. After left pneumonectomy gas exchange appeared to have improved. This was shown by improved arterial oxygen pressures during all steps of exercise in a cycle ergometer test in comparison with values obtained before surgery. This improvement could be entirely attributed to a decrease in physiological dead space ventilation.
Informed consent and communication of risk from radiological and nuclear medicine examinations: how to escape from a communication inferno
Authors: Eugenio Picano
Journal: BMJ (2004)

<i>Radiological and nuclear medicine examinations confer a definite (albeit low) long term risk of cancer, but patients undergoing such examinations often receive no or inaccurate information about these risks. Picano argues that this disregard of patient autonomy is no longer acceptable and suggests a practicable way of communicating risk</i>
The new tumor-suppressor gene inhibitor of growth family member 4 (ING4) regulates the production of proangiogenic molecules by myeloma cells and suppresses hypoxia-inducible factor-1 α (HIF-1α) activity: involvement in myeloma-induced angiogenesis
Authors: Simona Colla, Sara Tagliaferri, Francesca Morandi, Paolo Lunghi, Gaetano Donofrio, Davide Martorana, Cristina Mancini, Mirca Lazzaretti, Laura Mazzera, Lara Ravanetti, Sabrina Bonomini, Luca Ferrari, Claudia Miranda, Marco Ladetto, Tauro Maria Neri, Antonino Neri, Angela Greco, Marcellina Mangoni, Antonio Bonati, Vittorio Rizzoli, Nicola Giuliani
Journal: Blood (2007)
Characterization of a highly negative and labile binding protein induced in Euglena gracilis by cadmium.
Authors: D J Gingrich, D N Weber, C F Shaw, J S Garvey, D H Petering
Journal: Environmental Health Perspectives (1986)

The physiochemical properties and physiological significance of the cadmium-binding protein (CdBP) of the algae Euglena gracilis have been studied. Following in vivo exposure of cells to 0.4 or 1.3 micrograms/mL of Cd2+, all the cytosolic Cd is bound to high molecular weight species. At 4.7 micrograms/mL, appreciable CdBP has formed in cells grown under illumination or in the dark. An analogous ZnBP could not be isolated from control or Zn-exposed (20 micrograms/mL) cells, but zinc and a trace of copper were bound to the CdBP when 2-mercaptoethanol (2-ME) is added to the homogenates of Cd-treated cells and the buffers used during isolation. The large pool of very low molecular weight zinc species previously reported is increased when cells are exposed to high cadmium levels. Two distinct species, BP-1 and BP-2 are resolved by ion-exchange chromatography on DEAE-Sephadex. Unusually high conductivities (25 and 40 mSiemen) are required to displace them, indicating that they are very negatively charged proteins at pH 8.6. The pH for half-titration of bound Cd2+ is between 5 and 6. EDTA (0.4 M) and the CdBP isolated by gel-exclusion chromatography react biphasically with pseudo-first-order rate constants of 4 +/- 3 X 10(-4) sec-1 and 7 +/- 2 X 10(-5) sec-1. Neither form of the CdBP cross-reacts with antibodies to rat liver metallothionein (MT) antibodies. The structural, chemical, and functional differences between the Euglena CdBPs and mammalian MTs are discussed.(ABSTRACT TRUNCATED AT 250 WORDS)