tbuckley/cabot-search huggingface dataset:
In-Hospital Cardiopulmonary Resuscitation
Authors: George E. Taffet, Thomas A. Teasdale, Robert J. Luchi
Journal: JAMA (1988)

A retrospective review of 399 cardiopulmonary resuscitation (CPR) efforts in 329 veterans was performed to evaluate the observation that few geriatric patients were discharged alive after they underwent CPR. Cardiopulmonary resuscitation efforts with witnessed arrests were more frequently successful than efforts with unwitnessed arrests (47.7% vs 29.9%) and resulted in live discharge more often than efforts with unwitnessed arrests. Cardiopulmonary resuscitation efforts that resulted in a live discharge were more brief and involved a lower mean number of medication doses. Of the 77 CPR efforts in patients 70 years of age or older who had arrests, 24 (31%) were successful, and in 22 (92%), patients were alive after 24 hours. None lived to discharge. There were 322 CPR efforts in the younger cohort; 137 (43%) were successful, in 124 (91%) of these 137 efforts, patients were alive after 24 hours, and in 22 (16%), patients were discharged alive. Older patients were significantly less likely to live to discharge both at the time of arrest and 24 hours after successful resuscitation. When a multivariate analysis was used, the presence of sepsis, cancer, increased age, increased number of medication doses administered, and absence of witness were all "predictive" of poor outcome. Cardiopulmonary resuscitation should be administered only to those who have the greatest potential benefit from this emotionally and physically traumatic procedure.A review of 399 resuscitation efforts in 329 patients within one year at the Houston Veterans Administration Medical Center indicated that an age of 70 years or greater is associated with poor outcome after in-hospital cardiopulmonary resuscitation (CPR). Basing their conclusions on a detailed analysis of the methods and results of their study, the authors argue that CPR should be reserved for those who have a reasonable chance of survival until discharge, while admitting that the definition of this standard will vary. They recommend that patients 70 years or older, and patients with cancer or sepsis, should be identified as candidates for CPR only after considerable reflection by families and clinicians.
Abstract 2379: No Association of <i>PLIN</i> Polymorphisms with Hemorrhagic and Ischemic Strokes
Authors: Weihua Song, Jingzhou Chen, kai Sun, Hui Yu, Rutai Hui
Journal: Circulation (2007)

Background and Purpose Perilipin is a family of proteins that coat the intracellular lipid droplets and expressed in adipocytes, steroid-producing cells and atherosclerotic lesions. I t has been linked to the formation of foam cells and rupture of atherosclerotic plaques. To our knowledge, no other studies have investigated the association between polymorphic variation in PLIN and stroke. We hypothesized that genetic variations in PLIN might contribute to the susceptibility to stroke. We tested the hypothesis in two case-control studies. Methods Six PLIN tag SNPs (rs7176403, rs8179078, rs6496589, rs8179043, rs894160 , rs1052700,) were genotyped in 1571 stroke patients (690 cerebral thrombosis, 429 lacunar infarction, 452 intracerebral hemorrhage) and 1638 controls, by polymerase chain reaction (PCR) followed by ligase detection reaction (LDR) in combination with sequencing, and by PCR and restriction fragment length polymorphism. A SHEsis software was used to analyze pairwise linkage disequilibrium, and haplotype association. The results were confirmed in another independent case-control study, with 120 stroke patients and 240 controls. Results No association was found between the PLIN variants and stroke in the first study (P&gt;0.05). Six common haplotypes were identified within the study population, none of which was associated with stroke and all its subtypes (P&gt;0.05). The findings were confirmed in the second study (P&gt;0.05). Conclusions The data represent an important negative finding and that the common variants studied here do not have a major influence on susceptibility to stroke, even if perilipin has been linked to the formation of foam cell and rupture of human atherosclerotic plaques.
TCT-684 Impact Of Mixed Aortic Valve Stenosis On VARC-2 Outcomes And Post-Procedural Peri-Prosthetic Aortic Regurgitation In Patients Undergoing Transcatheter Aortic Valve Implantation: Results From The International Multicentric Study PRAGMATIC (Pooled Rotterdam – Milan – Toulouse In Collaboration)
Authors: Gennaro Giustino, Alaide Chieffo, Nicolas M. Van Mieghem, Didier Tchetche, Nicolas DUMONTEIL, Robert M. van der Boon, Bertrand Marcheix, Patrick W. Serruys, Damien Millischer, Didier Carrié, Peter De Jaegere, Antonio Colombo
Journal: Journal of the American College of Cardiology (2014)
Law and regulation of benzene.
Authors: I L Feitshans
Journal: Environmental Health Perspectives (1989)

OSHA has created final benzene regulations after extensive rulemakings on two occasions, 1978 and 1987. These standards have been the subject of extensive litigation for nearly 20 years. This article examines in detail the conceptual underpinnings of the Benzene Case, (which was decided by the U.S. Supreme Court in 1980) in light of U.S. administrative law precedents that have set limits upon administrative discretion under the test for "substantial evidence" and the "hard look doctrine." This article also addresses recent developments in the wake of the Benzene Case and their implications for benzene regulations following the "significant risk" doctrine in that case. This article briefly describes other national, regional, and international laws governing the use of benzene. This article concludes that the revisions of the benzene regulation and subsequent rulemaking provide substantial evidence of scientific underpinnings for regulatory action and that laws from other nations reflect an international consensus that occupational exposure to benzene is a proper subject of regulation. Such regulations and policies are therefore likely to withstand scrutiny and remain enforceable as widely accepted norms.
Heliox Improves Oxygen Delivery and Utilization during Dynamic Exercise in Patients with Chronic Obstructive Pulmonary Disease
Authors: Gaspar R. Chiappa, Fernando Queiroga, Ethiane Meda, Leonardo F. Ferreira, Fernando Diefenthaeler, Marcos Nunes, Marco A. Vaz, Maria Christina L. Machado, Luis Eduardo Nery, J. Alberto Neder
Journal: American Journal of Respiratory and Critical Care Medicine (2009)

Rationale: Normoxic heliox (mixture of 79% He and 21% O2) may enhance exercise tolerance in patients with chronic obstructive pulmonary disease (COPD). It remains to be determined whether part of these beneficial effects could be ascribed to increased O2 delivery (O2DEL) to locomotor muscles.Objectives: To investigate the effects of heliox on peripheral O2DEL and utilization during exercise in moderate to severe COPD.Methods: Twelve mildly hypoxic or nonhypoxemic men (FEV1 = 45.0 ± 13.0% predicted) underwent constant-work rate tests (70–80% peak) to the limit of tolerance while receiving heliox or room air. Near-infrared spectroscopy determined changes (Δ) in leg muscle deoxygenation (deoxyhemoglobin concentration [HHb], an index of fractional O2 extraction), and surface electromyography estimated muscle fiber recruitment (n = 5). Q̇ and SpO2 were monitored by impedance cardiography and pulse oximetry, respectively.Measurements and Main Results: Heliox significantly decreased dynamic hyperinflation and increased exercise tolerance compared with room air (640 ± 95 s vs. 371 ± 100 s; P < 0.01). Heliox also accelerated on-exercise dynamics of Q̇, which were accompanied by faster O2 uptake kinetics and slower Δ[HHb] responses (P < 0.05). During steady-state exercise, SpO2-corrected Δ[HHb] values decreased with heliox despite no significant changes in cardiac output. Muscle fiber recruitment and leg effort scores were also diminished (P < 0.05). On a multiple regression analysis, reductions in dynamic hyperinflation, dyspnea, and Δ[HHb] were independently related to improvements in exercise tolerance with heliox (R2 = 0.91; P < 0.01).Conclusions: Heliox increases lower limb O2DEL and utilization during dynamic exercise in patients with moderate to severe COPD. These effects enhance exercise tolerance in this patient population.
Desmosterol Deposition in Human and Experimental Atherosclerosis
Authors: JAMES H. HERNDON, MARVIN D. SIPERSTEIN
Journal: Circulation Research (1963)

The role of desmosterol in the production of atherosclerotic plaques has been studied. By means of gas chromatographic analysis, it has been possible for the first time to show that in patients treated with triparanol, even for short periods of time, desmosterol does contribute to the sterol deposition. Furthermore, in the induced atherosclerotic plaques of rabbits desmosterol has been found to deposit at least as readily as does cholesterol. It is concluded from these observations that the replacement of serum cholesterol with desmosterol does not seem to offer a rational approach to the treatment of atherosclerosis.
Transient Receptor Potential Channels Contribute to Pathological Structural and Functional Remodeling After Myocardial Infarction
Authors: Catherine A. Makarewich, Hongyu Zhang, Jennifer Davis, Robert N. Correll, Danielle M. Trappanese, Nicholas E. Hoffman, Constantine D. Troupes, Remus M. Berretta, Hajime Kubo, Muniswamy Madesh, Xiongwen Chen, Erhe Gao, Jeffery D. Molkentin, Steven R. Houser
Journal: Circulation Research (2014)

The cellular and molecular basis for post-myocardial infarction (MI) structural and functional remodeling is not well understood.Our aim was to determine if Ca2+ influx through transient receptor potential canonical (TRPC) channels contributes to post-MI structural and functional remodeling.TRPC1/3/4/6 channel mRNA increased after MI in mice and was associated with TRPC-mediated Ca2+ entry. Cardiac myocyte-specific expression of a dominant-negative (loss-of-function) TRPC4 channel increased basal myocyte contractility and reduced hypertrophy and cardiac structural and functional remodeling after MI while increasing survival in mice. We used adenovirus-mediated expression of TRPC3/4/6 channels in cultured adult feline myocytes to define mechanistic aspects of these TRPC-related effects. TRPC3/4/6 overexpression in adult feline myocytes induced calcineurin (Cn)-nuclear factor of activated T-cells (NFAT)-mediated hypertrophic signaling, which was reliant on caveolae targeting of TRPCs. TRPC3/4/6 expression in adult feline myocytes increased rested state contractions and increased spontaneous sarcoplasmic reticulum Ca2+ sparks mediated by enhanced phosphorylation of the ryanodine receptor. TRPC3/4/6 expression was associated with reduced contractility and response to catecholamines during steady-state pacing, likely because of enhanced sarcoplasmic reticulum Ca2+ leak.Ca2+ influx through TRPC channels expressed after MI activates pathological cardiac hypertrophy and reduces contractility reserve. Blocking post-MI TRPC activity improved post-MI cardiac structure and function.
Favorable Response to Neoadjuvant Chemotherapy and Radiation in a Patient With Prostatic Stromal Sarcoma
Authors: Adam C. Reese, Mark W. Ball, Jonathan E. Efron, Alex Chang, Christian Meyer, Trinity J. Bivalacqua
Journal: Journal of Clinical Oncology (2012)

A 66-year-old African American man initially presented to his local urologist with obstructive lower urinary tract symptoms.Digital rectal examination was performed and revealed an enlarged prostate without palpable nodules.The serum prostate-specific antigen concentration was 3.5 ng/mL.A transrectal, ultrasound-guided prostate biopsy was negative for cancer.The obstructive urinary symptoms of the patient were managed with tamsulosin and finasteride, and his prostate-specific antigen remained stable over the next several years.Six years later, the patient developed acute urinary retention for which a Foley catheter was placed.A computed tomography (CT) scan of the abdomen and pelvis revealed a 9 ϫ 10 ϫ 8-cm prostatic mass protruding into the bladder (Fig 1).A repeat prostate biopsy was not performed.The local urologist of the patient suspected a bladder outlet obstruction from benign prostatic hyperplasia and recommended a robotic-assisted suprapubic prostatectomy.A subtotal prostatectomy was performed robotically.Pathology from this resection revealed a high-grade (grade 3 of 3) prostatic stromal sarcoma with positive surgical margins.The prostate specimen weighed 154 g.The patient was referred to our institution for additional management.Cross-sectional imaging revealed persistent prostatic enlargement but no evidence of distant disease.Because of the incompletely resected sarcoma and violation of the tumor capsule, an aggressive management strategy including neoadjuvant chemotherapy and radiation followed by radical cystoprostatectomy was recommended.The patient received two cycles of neoadjuvant ifosfamide and adriamycin followed by 50 Gy of intensity-modulated radiation therapy.Follow-up CT of the abdomen and pelvis revealed a
Activated transcription factor nuclear factor-kappa B is present in the atherosclerotic lesion.
Authors: K Brand, S Page, G Rogler, A Bartsch, R Brandl, R Knuechel, M Page, C Kaltschmidt, P A Baeuerle, D Neumeier
Journal: Journal of Clinical Investigation (1996)

Nuclear factor-kappa B (NF-kappaB)/Rel transcription factors play an important role in the inducible regulation of a variety of genes involved in the inflammatory and proliferative responses of cells. The present study was designed to elucidate the implication of NF-kappaB/Rel in the pathogenesis of atherosclerosis. Activation of the dimeric NF-kappaB complex is regulated at a posttranslational level and requires the release of the inhibitor protein IkappaB. The newly developed mAb alpha-p65mAb recognizes the IkappaB binding region on the p65 (RelA) DNA binding subunit and therefore selectively reacts with p65 in activated NF-kappaB. Using immunofluorescence and immunohistochemical techniques, activated NF-kappaB was detected in the fibrotic-thickened intima/media and atheromatous areas of the atherosclerotic lesion. Activation of NF-kappaB was identified in smooth muscle cells, macrophages, and endothelial cells. Little or no activated NF-kappaB was detected in vessels lacking atherosclerosis. Electrophoretic mobility shift assays and colocalization of activated NF-kappaB with NF-kappaB target gene expression suggest functional implications for this transcription factor in the atherosclerotic lesion. This study demonstrates the presence of activated NF-kappaB in human atherosclerotic tissue for the first time. Atherosclerosis, characterized by features of chronic inflammation and proliferative processes, may be a paradigm for the involvement of NF-kappaB/Rel in chronic inflammatory disease.
Stroke, Orthostatic Hypotension, and Focal Seizures
Authors: Terrence L. Riley
Journal: JAMA (1981)

A 75-year-old man had development of left hemiparesis after a cerebral infarction. Nine months later, he was admitted to the hospital after generalized tonic clonic convulsion. In the hospital, he had clonic movement on the left side of the body. Even after acceptable control of orthostatic hypotension, rising from supine to standing position evoked slow waves over the right hemisphere on the EEG tracing. This example of focal seizures with orthostatic hypotension shows that previously compromised cerebral tissue or vessels may be vulnerable to changes in blood pressure. We suggest that convulsive movements associated with hypotension or syncope result from cortical mechanisms rather than brainstem tonic release mechanisms.
Vascular Endothelial Growth Factor Overexpression in Ischemic Skeletal Muscle Enhances Myoglobin Expression In Vivo
Authors: Vincent van Weel, Martine M.L. Deckers, Jos M. Grimbergen, Kees J.M. van Leuven, JanWillem H.P. Lardenoye, Reinier O. Schlingemann, Geerten P. van Nieuw Amerongen, J. Hajo van Bockel, Victor W.M. van Hinsbergh, Paul H.A. Quax
Journal: Circulation Research (2004)

Therapeutic angiogenesis using vascular endothelial growth factor (VEGF) is considered a promising new therapy for patients with arterial obstructive disease. Clinical improvements observed consist of improved muscle function and regression of rest pain or angina. However, direct evidence for improved vascularization, as evaluated by angiography, is weak. In this study, we report an angiogenesis-independent effect of VEGF on ischemic skeletal muscle, ie, upregulation of myoglobin after VEGF treatment. Mice received intramuscular injection with adenoviral VEGF-A or either adenoviral LacZ or PBS as control, followed by surgical induction of acute hindlimb ischemia at day 3. At day 6, capillary density was increased in calf muscle of Ad.VEGF-treated versus control mice (P<0.01). However, angiographic score of collateral arteries was unchanged between Ad.VEGF-treated and control mice. More interestingly, an increase in myoglobin was observed in Ad.VEGF-treated mice. Active myoglobin was 1.5-fold increased in calf muscle of Ad.VEGF-treated mice (P< or =0.01). In addition, the number of myoglobin-stained myofibers was 2.6-fold increased in Ad.VEGF-treated mice (P=0.001). Furthermore, in ischemic muscle of 15 limb amputation patients, VEGF and myoglobin were coexpressed. Finally, in cultured C2C12 myotubes treated with rhVEGF, myoglobin mRNA was 2.8-fold raised as compared with PBS-treated cells (P=0.02). This effect could be blocked with the VEGF receptor tyrosine kinase inhibitor SU5416. In conclusion, we show that VEGF upregulates myoglobin in ischemic muscle both in vitro and in vivo. Increased myoglobin expression in VEGF-treated muscle implies an improved muscle oxygenation, which may, at least partly, explain observed clinical improvements in VEGF-treated patients, in the absence of improved vascularization.
Blood Level Warning Device
Authors: H. E. Bell
Journal: BMJ (1967)

March 1'967 Correspondence thyrotoxicosis and taking chlordiazepoxide the T3 uptake value lay in the normal (or low normal) range, and the "'I tracei test showed depressed thyroid uptake.We can find no mention of this effect in the literature and feel it appropriate to draw attention to it.The suggestion (as put forward for some other drugs-for example, contraceptive pills) that chiordiazepoxide may interfere with the dissociation of protein-bound thyroxine into free thyroxine could explain the lowered T3 uptake, but not the depressed thyroid "'I uptake.We therefore think It possible that chlor- diazepoxide acts as an antithyroid drug (this could explain both effects)..-I am, etc.,
465. In Vivo Selection of Genetically Modified Primary Human Hematopoietic Cells Using a Cell Growth Switch
Authors: Linlin Wang, Yasuo Nagasawa, Brent Wood, Ingrid Lintmaer, Thalia Papayannopoulou, Michael Harkey, Cynthia Nougirat, C. Anthony Blau
Journal: Molecular Therapy (2005)

Methods for regulating the growth of transplanted cells may have many applications in gene and cell therapy. One such method uses conditional signaling molecules that can be activated in response to artificial ligands called chemical inducers of dimerization (CIDs). Here we examine the response of human cord blood cells to a CID-triggered growth signal, in vivo. CD34+ cells transduced with a lentivirus vector encoding a derivative of the thrombopoietin receptor (F36VMpl) and green fluorescent protein (GFP) were transplanted into immune deficient mice. CID treatment was associated with a >12 – fold expansion of GFP+ CD71+ erythroid cells that were localized mainly in the marrow, and a unique subset of multipotential and erythroid progenitors that were confined to the spleen. Both the CD71+ cells and the progenitor colonies were intensely GFP+. The CID response was oligoclonal, with most colonies containing a single transgene copy. Despite expressing F36Vmpl, GFP+ B lymphoid and myeloid cells showed no response. CID-responsive progenitors and CD71+ cells were detectable for up to 5 weeks following the end of CID; however these effects were not sustained in secondary transplant recipients. These findings establish CIDs as growth factors for genetically modified human hematopoietic cells.
INQUIRY INTO THE PROPRIETY OF OPENING THE BOWELS SOON AFTER THE OPERATION FOR STRANGULATED HERNIA
Authors: J. S. Gamgee
Journal: BMJ (1854)

OtrnMWNICATIONS. 57vith blood and muc.Ie had no pain, and felt comfort able; the enema was repeated. 31t.The bowels had not been moved; he felt more eomfortable in every respect.
Effects of cimetidine and ranitidine on high density lipoprotein cholesterol concentrations.
Authors: J A Wilson, I F Craig
Journal: BMJ (1985)

To assess the effect of cimetidine and ranitidine on high density lipoprotein (HDL) cholesterol concentration two groups of eight patients with duodenal ulcer or oesophagitis matched for age, sex, and cigarette consumption were given either cimetidine 1 g daily or ranitidine 300 mg daily for one month. There was no significant change in the cholesterol content of HDL and its subfraction HDL3 after treatment with ranitidine or cimetidine, or in the cholesterol content of the subfraction HDL2 after treatment with ranitidine; the HDL2 cholesterol concentration was, however, significantly increased after treatment with cimetidine. Further studies are being undertaken to establish the mechanism of this effect.
Communicating with Patients Who Cannot Read
Authors: Barry D. Weiss, Cathy Coyne
Journal: New England Journal of Medicine (1997)

In 1992, the Department of Education tested 26,000 adults in the National Adult Literacy Survey to assess the literacy of the U.S. population in the English language.1 On the basis of the survey results, it was estimated that 40 million to 44 million people, or about one quarter of the adult population in the United States, cannot understand written materials that require only very basic proficiency in reading. These people would generally be unable to read and understand instructions on medication bottles or household cleaning solutions, notes from a child's teacher, or directions on a map.Poor reading skills are . . .
Microbe sampling by mucosal dendritic cells is a discrete, MyD88-independent stepin Δ<i>invG S</i>. Typhimurium colitis
Authors: Siegfried Hapfelmeier, Andreas J. Müller, Bärbel Stecher, Patrick Kaiser, Manja Barthel, Kathrin Endt, Matthias Eberhard, Riccardo Robbiani, Christoph A. Jacobi, Mathias Heikenwalder, Carsten Kirschning, Steffen Jung, Thomas Stallmach, Marcus Kremer, Wolf-Dietrich Hardt
Journal: The Journal of Experimental Medicine (2008)

Intestinal dendritic cells (DCs) are believed to sample and present commensal bacteria to the gut-associated immune system to maintain immune homeostasis. How antigen sampling pathways handle intestinal pathogens remains elusive. We present a murine colitogenic Salmonella infection model that is highly dependent on DCs. Conditional DC depletion experiments revealed that intestinal virulence of S. Typhimurium SL1344 ΔinvG mutant lacking a functional type 3 secretion system-1 (ΔinvG)critically required DCs for invasion across the epithelium. The DC-dependency was limited to the early phase of infection when bacteria colocalized with CD11c+CX3CR1+ mucosal DCs. At later stages, the bacteria became associated with other (CD11c−CX3CR1−) lamina propria cells, DC depletion no longer attenuated the pathology, and a MyD88-dependent mucosal inflammation was initiated. Using bone marrow chimeric mice, we showed that the MyD88 signaling within hematopoietic cells, which are distinct from DCs, was required and sufficient for induction of the colitis. Moreover, MyD88-deficient DCs supported transepithelial uptake of the bacteria and the induction of MyD88-dependent colitis. These results establish that pathogen sampling by DCs is a discrete, and MyD88-independent, step during the initiation of a mucosal innate immune response to bacterial infection in vivo.