tbuckley/cabot-search huggingface dataset:
Stability and explicitness: In defense of implicit representation
Authors: Axel Cleeremans, Luis Jiménez
Journal: Behavioral and Brain Sciences (1999)

Stability of activation, while it may be necessary for information to become available to consciousness, is not sufficient to produce phenomenal experience. We suggest that consciousness involves access to information and that access makes information symbolic. From this perspective, implicit representations exist, and are best thought of as subsymbolic. Crucially, such representations can be causally efficacious in the absence of consciousness.
Immunological and functional differences between human type I and II colony-stimulating factors.
Authors: M C Wu, A M Miller, A A Yunis
Journal: Journal of Clinical Investigation (1981)

Two distinct types of colony-stimulating factor (CSF) have recently been described in human tissues and cultured cell lines. Antisera to purified type I and II CSF were prepared in rabbits. Anti-CSF I antibody inhibits CSF I, but has no effect on CSF II. It cross-inhibits CSF I from several other human sources, but does not inhibit CSF from mouse lung or mouse L cells. Anti-CSF II antibody inhibits the activity of CSF II, but has no effect on CSF I. A radioimmunoassay for CSF I has been established. Competitive binding assay further demonstrated the immunological differences between CSF I and II. When CSF II is used to stimulate human marrow cells fractionated by sedimentation velocity, two populations of CFU-C are separated, one sedimenting at 8 mm/h and forming colonies by day 7, and a second sedimenting at 6.8 mm/h and forming colonies by day 13. In contrast, CSF I does nt stimulate colony growth by day 7 but does do so by day 13 in cells sedimenting between 7.2-8.5 mm/h. These results indicate that CSF I and II are distinct in their biochemical, immunological, and functional properties.
Acute coronary syndrome: unstable angina and non-ST segment elevation myocardial infarction
Authors: E. D Grech
Journal: BMJ (2003)

The term acute coronary syndrome refers to a range of acute myocardial ischaemic states. It encompasses unstable angina, non-ST segment elevation myocardial infarction (ST segment elevation generally absent), and ST segment elevation infarction (persistent ST segment elevation usually present). This article will focus on the role of percutaneous coronary intervention in the management of unstable angina and non-ST segment elevation myocardial infarction; the next article will address the role of percutaneous intervention in ST segment elevation infarction.

Although there is no universally accepted definition of unstable angina, it has been described as a clinical syndrome between stable angina and acute myocardial infarction. This broad definition encompasses many patients presenting with varying histories and reflects the complex pathophysiological mechanisms operating at different times and with different outcomes. Three main presentations have been described—angina at rest, new onset angina, and increasing angina.



Spectrum of acute coronary syndromes according to electrocardiographic and biochemical markers of myocardial necrosis (troponin T, troponin I, and creatine kinase MB), in patients presenting with acute cardiac chest pain



The process central to the initiation of an acute coronary syndrome is disruption of an atheromatous plaque. Fissuring or rupture of these plaques—and consequent exposure of core constituents such as lipid, smooth muscle, and foam cells—leads to the local generation of thrombin and deposition of fibrin. This in turn promotes platelet aggregation and adhesion and the formation of intracoronary thrombus.



Diagram of an unstable plaque with superimposed luminal thrombus



Unstable angina and non-ST segment elevation myocardial infarction are generally associated with white, platelet-rich, and only partially occlusive thrombus. Microthrombi can detach and embolise downstream, causing myocardial ischaemia and infarction. In contrast, ST segment elevation (or Q wave) myocardial infarction has red, fibrin-rich, and more stable occlusive thrombus.



Distal embolisation of a platelet-rich thrombus causing occlusion of intramyocardial arteriole (arrow). Such …
Expression of 92-kD type IV collagenase/gelatinase (gelatinase B) in osteoarthritic cartilage and its induction in normal human articular cartilage by interleukin 1.
Authors: M Mohtai, R L Smith, D J Schurman, Y Tsuji, F M Torti, N I Hutchinson, W G Stetler-Stevenson, G I Goldberg
Journal: Journal of Clinical Investigation (1993)

We report here that a 92-kD gelatinolytic metalloproteinase is expressed as protein and mRNA in human osteoarthritic cartilage, but not in normal adult articular cartilage. Western immunoblotting demonstrated that the 92-kD gelatinolytic activity corresponded to 92-kD type IV collagenase/gelatinase (gelatinase B); mRNA for gelatinase B was identified by Northern blotting. Chondrocytes from normal cartilage also exhibited mRNA for 72-kD type IV collagenase/gelatinase (gelatinase A), tissue collagenase, and stromelysin-1, and these mRNAs were increased in osteoarthritic cartilage. Regional analysis of osteoarthritic cartilage samples from four individuals revealed that gelatinase B mRNA was expressed in grossly fibrillated areas; two of four nonfibrillated cartilage samples failed to exhibit the mRNA, but did have increased levels of mRNA for other neutral metalloproteinases. IL-1 alpha treatment of normal human cartilage explants or isolated chondrocytes induced increased levels of gelatinase B and increased mRNA for tissue collagenase and stromelysin-1. Under identical conditions, mRNA levels for gelatinase A were not increased indicating that regulation of this enzyme in human articular chondrocytes is distinct from that of other metalloproteinases. Our data showing expression of gelatinase B in fibrillated cartilage suggest that it is a marker of progressive articular cartilage degradation in osteoarthritis.
Functional and Bioenergetic Consequences of Postinfarction Left Ventricular Remodeling in a New Porcine Model
Authors: Jianyi Zhang, Norbert Wilke, Ying Wang, Yi Zhang, Chunshen Wang, Marcel H.J. Eijgelshoven, Yong K. Cho, Yo Murakami, Kamil Ugurbil, Robert J. Bache, Arthur H.L. From
Journal: Circulation (1996)

Background The underlying mechanisms by which left ventricular remodeling (LVR) leads to congestive heart failure (CHF) are unclear. This study examined the functional and bioenergetic abnormalities associated with postinfarction ventricular remodeling in a new, large animal model. Methods and Results Remodeling was induced by circumflex coronary artery ligation in young pigs. LV mass, volume, ejection fraction (EF), the ratio of scar surface area to LV surface area, and LV wall stresses were calculated from magnetic resonance imaging anatomic data and simultaneously measured LV pressure. Hemodynamics, transmural blood flow, and high-energy phosphates (spatially localized 31 P–nuclear magnetic resonance) were measured under basal conditions, during hyperperfusion induced by pharmacological vasodilation with adenosine, and during pyruvate infusion (11 mg/kg per minute IV). Six of 18 animals with coronary ligation developed clinical CHF while the remaining 12 animals had LV dilation (LVR) without CHF. The results were compared with 16 normal animals. EF decreased from 55.9±5.6% in normals to 34.6±2.3% in the LVR group ( P &lt;.05) and 24.2±2.8% in the CHF group ( P &lt;.05 versus LVR). The infarct scar was larger in CHF hearts than in LVR hearts ( P &lt;.05). In normals, LV myocardial creatine phosphate (CP)/ATP ratios were 2.10±0.10, 2.06±0.16, and 1.92±0.12 in subepicardium (EPI), mid myocardium (MID), and subendocardium (ENDO), respectively. In LVR hearts, the corresponding ratios were decreased to 1.99±0.13, 1.80±0.14, and 1.57±0.15 (ENDO P &lt;.05 versus normal). In CHF hearts, CP/ATP ratios were 1.41±0.14, 1.33±0.15, and 1.25±0.15; ( P &lt;.05 versus LVR in EPI and MID). The calculated myocardial free ADP levels were significantly increased only in CHF hearts. Conclusions Bioenergetic abnormalities in remodeled myocardium are related to the severity of LV dysfunction, which, in turn, is dependent on the severity of the initiating myocardial infarction.
Abstract 3383: Role of BHLHB3 regulation of p53 and c-Jun during the induction of cancer cell dormancy in a model of HNSCC
Authors: Paloma Bragado, Yeriel Estrada, Julio Aguirre-Ghiso
Journal: Cancer Research (2010)

Abstract Head and neck squamous cell carcinoma (HNSCC) is an aggressive cancer for which survival rates have improved marginally over the last 30 years. Majority of cancer patients will die of metastases that develop from disseminated tumor cells (DTCs). Using computational tools and the experimental model, HEp3 (HNSCC) cells, we have identified p53 and BHLHB3 as critical genes transcriptionally induced by p38α/β signaling and required for the induction of HEp3 cells quiescence in vivo. BHLHB3 is a transcriptional repressor and a regulator of the circadian rhythm. We have demonstrated that BHLHB3 upregulation is required for the quiescence of D-HEp3 cells. We further showed that overexpression of BHLHB3 in T-HEp3 cells inhibits proliferation and correlates with increase levels of p21 (cell cycle arrest marker and p53 target gene) in vivo. We next tested the possibility that BHLHB3 regulates p53 expression/activity. Our results show that overexpression of BHLHB3 in T-HEp3 cells induced p53 transcriptional activity of a p53-luciferase reporter construct and increased p53 protein levels in vitro. In addition, downregulation of BHLHB3 using RNA interference in D-HEp3 cells also reduced p53 protein levels in vitro. We had also demonstrated that p53 upregulation in dormant HNSCC D-HEp3 cells is dependent on c-Jun downregulation by p38α. Accordingly, BHLHB3 downregulation via RNAi in D-HEp3 cells correlates with an increase in c-jun expression in vitro, suggesting that BHLHB3 regulation of p53 may be mediated through c-Jun. We propose that induction of tumor cell quiescence by BHLHB3 may be mediated through p53 regulation, suggesting a strong crosstalk between both pathways for growth suppression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3383.
Compartment syndrome following an insect bite
Authors: A.V. Evans, A. Darvay, I.H. Jenkins, R. Russell-Jones
Journal: British Journal of Dermatology (2001)

Sir, We report a case of compartment syndrome caused by a streptococcal cellulitis complicating an insect bite. Compartment syndrome is defined as occurring when the circulation and function of tissues within a closed space are compromised by increased pressure within that space.1 A 52‐year‐old woman was bitten by an insect on the lateral aspect of the right elbow while on holiday in Corfu. She scratched the area, which became red and inflamed. Over the next week her arm became swollen and painful and she began to feel unwell. She was feverish (38·9 °C) with a tachycardia (120 bpm) and had a severe cellulitis of the right arm. Hand, wrist and elbow movements were reduced but this was attributed to the pain and swelling. Peripheral pulses and sensation were normal in the hand. Investigations revealed a neutrophilia of 15·6 × 109 L−1 (normal 2·0–7·5 × 109 L−1) and a C‐reactive protein of 240 g dL−1 (normal < 7 g dL−1). A plain X‐ray of the forearm was normal. Anti‐streptolysin‐O titre was found to be elevated at 640 units (normal < 200 units) and anti‐DNase was 3840 units (normal < 240 units), implying a streptococcal infection.
A memorable patient: Mental illness became real and personal
Authors: J. Hare
Journal: BMJ (1997)

Arthur was the object of some ridicule when I arrived on the ward as a fresh faced psychiatry SHO. He would stride up to the nursing station each morning attired in his pin stripe with accompanying umbrella and case. Requesting to pay his bill he also asked for a taxi to be called, for he was late for the office.

Arthur was a retired executive in his late sixties. He was a Sergeant Wilson of a man, an English gentleman, very likeable and seemingly quite mad.

Life had been good to Arthur, loving wife, …
Reversal of Cardiogenic Shock by Percutaneous Left Atrial-to-Femoral Arterial Bypass Assistance
Authors: Holger Thiele, Bernward Lauer, Rainer Hambrecht, Enno Boudriot, Howard A. Cohen, Gerhard Schuler
Journal: Circulation (2001)

Background — Recovery of myocardial function after revascularization of acutely occluded coronary arteries may require several days. During this critical time, patients in cardiogenic shock may have low output. A newly developed percutaneous left ventricular assist device (VAD) may offer effective treatment for these patients by providing active circulatory support. Methods and Results — Between May 2000 and May 2001, VADs were implanted in 18 consecutive patients who had cardiogenic shock after myocardial infarction. The device was connected to the patient’s circulation by insertion of a 21F venous cannula into the left atrium by transseptal puncture; blood was returned to the iliac artery through an arterial cannula. Mean duration of cardiac assistance was 4±3 days. Mean flow of the VAD was 3.2±0.6 L/min. Before support, cardiac index was 1.7±0.3 L/min per m 2 and improved to 2.4±0.6 L/min per m 2 ( P &lt;0.001). Mean blood pressure increased from 63±8 mm Hg to 80±9 mm Hg ( P &lt;0.001). Pulmonary capillary wedge pressure, central venous pressure, and pulmonary artery pressure were reduced from 21±4, 13±4, and 31±8 mm Hg to 14±4, 9±3, and 23±6 mm Hg (all P &lt;0.001), respectively. Overall 30-day mortality rate was 44%. Conclusions — A newly developed VAD can be rapidly deployed in the catheterization laboratory setting. This device provides up to 4.0 L/min of assisted cardiac output, which may aid to revert cardiogenic shock. The left ventricle is unloaded by diverting blood from the left atrium to the systemic circulation, making recovery more likely after an ischemic event. The influence of this device on long-term prognosis warrants further investigation.
Dietary Salt Intake and Blood Pressure
Authors: William E. Serafin
Journal: JAMA (1984)

To the Editor.—  The recent article by Holden and associates 1 does not contribute to the understanding of the relationship, if any, of dietary salt intake and hypertension because the methods and data are seriously flawed. The group of persons whose conditions were previously diagnosed as hypertension constituted 22% of the initial study sample but were excluded from analysis because their salt intake had been modified, presumably because of the diagnosis of hypertension. By excluding this group, the authors may have excluded many of the very persons who did become hypertensive because of an increased salt intake. Of course, there is no way of including these data because the matter being studied— salt intake—already had been modified by the diagnosis of hypertension. Furthermore, all studies of this nature must contend with the fact that the general population in our country is not naive to the dietary salt-hypertension hypothesis; this may
Abstract 5264: Are the methylation of MGMT (O6-methylguanine-DNA methyltransferase) and the DNA mismatch repair (MMR) mechanism frequently involved in pediatric cancers?
Authors: Aurelia Nguyen, Michele LEGRAIN, Agnès Neuville, Erwan Pencreach, Eric Guerin, Patrick Lutz, Marie Pierre Gaub, Dominique Guenot, Natacha Entz-Werlé
Journal: Cancer Research (2010)

Abstract In pediatric oncology more and more protocols are including now temozolomide (TMZ) as a drug in the first line treatment or at relapse time. MGMT activity is known to circumvent the toxicity of alkylating agents such as TMZ. The defect of MMR mechanism is involved also as a cellular way for cancers to resist to TMZ. Only few studies have been already done in the pediatric field focusing on the study of these markers of TMZ resistance. Based on the new therapeutic indications of this drug in pediatric cancers, we performed a study in 100 malignant pediatric tumors from various origins to evaluate the MGMT methylation and the MMR mechanism. Material and methods: 12 high grade gliomas (HGG), 13 medulloblastomas (MB), 15 osteosarcomas (OS), 15 Ewing sarcomas (EWS), 15 rhabdomyosarcomas (RMS), 15 NBs and 15 acute lymphoblastic leukemias (ALLs) were included retrospectively in the study. DNA was extracted from tumors at diagnosis. In all tumors, the methylated status of MGMT was analyzed by methylation specific PCR (MS-PCR). Simultaneously, its expression was studied by immunohistochemistry. To analyze the MMR status in each tumor, an allelotyping method was performed in these tumors by using the NIH recommended microsatellites. Results: Out of these 100 samples, 3 tumors (2 HGGs and 1 MB) were presenting a MSI (microsatellite instability), witness of a MMR deficiency. Only 5 tumors (2 EWSs, 2 HGGs and 1 MB) had a methylated MGMT promoter. One HGG was presenting both abnormalities at the same time. The immunohistochemical results were concordant with MS-PCR observations. Concerning the tumors treated with TMZ (12 HGGs, 4 MBs, 2 EWSs and 4 NBs), we do not observed any differences on survival between the unmethylated and methylated tumors. Discussion: Methylation of MGMT promoter and MMR deficiency are rare in pediatric tumors and therefore seem not to be the major mechanisms involved in the sensitivity to TMZ. Our results suggest that in pediatric tumors, other mechanisms for TMZ sensitivity or resistance should be activated. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5264.
Abstract 3164: Angioscopic Findings of Sirolimus-Eluting Stent for Acute Myocardial Infarction: An Intermediate-term Follow-up Study
Authors: Kazuoki Dai, Masaharu Ishihara, Ichiro Inoue, Takuji Kawagoe, Yuji Shimatani, Satoshi Kurisu, Yasuharu Nakama, Tatsuya Maruhashi, Eisuke Kagawa, Toshiyuki Aokage, Hiroki Ikenaga
Journal: Circulation (2007)

Background: Sirolimus-Eluting Stent (SES) is effective in reducing restenosis. Although several studies have reported the usefulness of SES in patients with acute myocardial infarction (AMI), the current major concerns of the use of SES in AMI are over-suppression of neointimal formation and late thrombosis. Coronary angioscopic examination provides an opportunity to assess neointimal coverage over stent and adherent thrombus in patients. Method: This study consisted of 18 patients who underwent primary angioplasty with SES for AMI. A mean average of 7.6 ± 2.5 months after SES implantation, coronary angioscopic examination was performed. Neointimal coverage of the SES was assessed by the grading as: grade 0 = complete exposure of the stent struts, grade 1 = dull light reflex from stent struts, grade 2 = no light reflex, but slightly visible stent struts, and grade 3 = complete coverage. Because the grade of neointimal coverage may vary from struts to struts, both maximum and minimum grade of neointimal coverage were assessed. The presence of thrombus was also evaluated. Results: All but one patient had at least 2 different grades of neointimal coverage; one patient had only grade 0. When the maximum grade of neointimal coverage was assessed, grade 0 was observed in 1 patient, grade 1 in 4 patients, grade 2 in 8 patients, and grade 3 in 5 patients. As to minimum grade, grade 0 was observed in 11 patients and grade 1 in 7 patients, however, grade 2 and 3 was not observed. Thrombus adherent to uncovered stent struts (grade 0 or 1) was observed in 8 patients (44%). Conclusion: The process of neointimal coverage over SES was heterogeneous. Even 7 months after SES implantation for AMI, most of the stent struts were not covered by neointimal with high incidence of adherent thrombus. Long-term aggressive anti-platelet therapy should be advocated for patients with AMI who were treated with SES.
If guns don't kill people, ignorance might
Authors: E. Davies
Journal: BMJ (2013)

President Obama had a lot to say about gun control in his state of the union address this week (doi:10.1136/bmj.f1034).

In a grand rhetorical flourish, he said that the victims of gun crime and their families deserved a Congressional vote on issues such as background checks, sales restrictions, and ammunition limits.

“In this chamber tonight [are] more than two dozen Americans whose lives have been torn apart by gun violence. They deserve a vote. Gabby Giffords deserves a vote. The families of Newtown deserve a vote. The families of Aurora deserve a vote. The families of Oak Creek, and Tucson, and Blacksburg, and …
CARDIAC ARREST AND RESUSCITATION DURING REPAIR OF DIAPHRAGMATIC HERNIA IN INFANT
Authors: Herbert Volk
Journal: JAMA (1952)

Cardiac arrest occurring during anesthesia or anesthesia and operation has been a not too uncommon complication, usually resulting in permanent damage to the brain or death.<sup>1</sup>Recently there has been a small but constantly increasing number of these cases in which the patient was treated successfully by cardiac massage. At the Presbyterian Hospital in New York City, during the four year period from January, 1947, to December, 1950, there have been 23 instances of cardiac arrest resulting in 12 deaths (57% mortality); however, during 1950, the last year of that four year period, of 8 instances of cardiac arrest, 6 patients (75%) were resuscitated and recovery was complete.<sup>1d</sup>The statistics for each year are presented in the table. The purpose of this paper is to present the case of what we believe is the youngest patient ever reported to have cardiac arrest with full recovery, to discuss the
Stress and CRF gate neural activation of BDNF in the mesolimbic reward pathway
Authors: Jessica J Walsh, Allyson K Friedman, Haosheng Sun, Elizabeth A Heller, Stacy M Ku, Barbara Juarez, Veronica L Burnham, Michelle S Mazei-Robison, Deveroux Ferguson, Sam A Golden, Ja Wook Koo, Dipesh Chaudhury, Daniel J Christoffel, Lisa Pomeranz, Jeffrey M Friedman, Scott J Russo, Eric J Nestler, Ming-Hu Han
Journal: Nature Neuroscience (2013)
Defective Neurogenesis in Citron Kinase Knockout Mice by Altered Cytokinesis and Massive Apoptosis
Authors: Ferdinando Di Cunto, Sara Imarisio, Emilio Hirsch, Vania Broccoli, Alessandro Bulfone, Antonio Migheli, Cristiana Atzori, Emilia Turco, Roberta Triolo, Gian Paolo Dotto, Lorenzo Silengo, Fiorella Altruda
Journal: Neuron (2000)
Mosaicism of activatingFGFR3 mutations in human skin causes epidermal nevi
Authors: C. Hafner
Journal: Journal of Clinical Investigation (2006)

Epidermal nevi are common congenital skin lesions with an incidence of 1 in 1,000 people; however, their genetic basis remains elusive. Germline mutations of the FGF receptor 3 (FGFR3) cause autosomal dominant skeletal disorders such as achondroplasia and thanatophoric dysplasia, which can be associated with acanthosis nigricans of the skin. Acanthosis nigricans and common epidermal nevi of the nonorganoid, nonepidermolytic type share some clinical and histological features. We used a SNaPshot multiplex assay to screen 39 epidermal nevi of this type of 33 patients for 11 activating FGFR3 point mutations. In addition, exon 19 of FGFR3 was directly sequenced. We identified activating FGFR3 mutations, almost exclusively at codon 248 (R248C), in 11 of 33 (33%) patients with nonorganoid, nonepidermolytic epidermal nevi. In 4 of these cases, samples from adjacent histologically normal skin could be analyzed, and FGFR3 mutations were found to be absent. Our results suggest that a large proportion of epidermal nevi are caused by a mosaicism of activating FGFR3 mutations in the human epidermis, secondary to a postzygotic mutation in early embryonic development. The R248C mutation appears to be a hot spot for FGFR3 mutations in epidermal nevi.