tbuckley/cabot-search huggingface dataset:
Defining the architecture of the red blood cell membrane: Newer biophysical approaches
Authors: Stephen B. Shohet, Stephen E. Bicknese
Journal: American Journal of Hematology (1993)

Abstract For many years the red cell membrane has served as an extraordinarily valuable model for membrane structure and function. During the past 2 decades, the biochemical concept of the membrane skeleton was established, and, with the help of electron microscopy, a partial depiction of this structure evolved. Newer biophysical approaches designed to measure distances between various components of membrane skeleton as well as distances between the membrane skeleton and the overlying bilayer should now help to define this structure more realistically. Fluorescence resonance energy transfer, single photon radioluminescence, and total internal reflectance are three biophysical techniques that will enable us to measure such distances over a substantial range, which extends from a few Angstroms to ∼2 μm. The ability to make such measurements in intact cells and in fully hydrated, undenatured membrane preparations should add a new dimension to our understanding of the structure of the red cell membrane. © 1993 Wiley‐Liss, Inc.
Lipid IVA inhibits synthesis and release of tumor necrosis factor induced by lipopolysaccharide in human whole blood ex vivo.
Authors: N L Kovach, E Yee, R S Munford, C R Raetz, J M Harlan
Journal: The Journal of Experimental Medicine (1990)

Tumor necrosis factor (TNF) released by lipopolysaccharide (LPS)-stimulated mononuclear phagocytes is a critical mediator of sepsis. We examined the capacities of rough mutant Salmonella typhimurium LPS (Rc) and LPS partial structures lipid A, monophosphoryl lipid A (MPLA), lipid IVA, and lipid X to induce production of TNF in whole blood. Rc LPS (0.0001-10 ng/ml) produced a dose-dependent release of TNF as determined by cytotoxicity of actinomycin D-sensitized L929 murine fibroblasts. Lipid A, MPLA, lipid IVA, and lipid X exhibited decreasing capacities to stimulate production of TNF in whole blood, respectively. Fractional deacylation of LPS by incubation with acyloxyacyl hydrolase isolated from human leukocytes produced a reduction in the capacity of LPS to induce TNF release in whole blood. Maximal enzymatic deacylation reduced activity of LPS by greater than 100-fold. Coincubation with lipid IVA inhibited TNF release induced by Rc LPS or lipid A, but not by phorbol ester. In contrast, MPLA, lipid X, and deacylated LPS failed to inhibit LPS-stimulated release of TNF. Corresponding to the inhibition of the release of TNF protein, lipid IVA also inhibited the accumulation of TNF mRNA in LPS-stimulated mononuclear cells. These results suggest that lipid IVA may act as a competitive antagonist of LPS, perhaps at the receptor level.
Hospital stays for young adults with flu shot up in England in 2009
Authors: S. Mayor
Journal: BMJ (2010)

Hospitalisation rates for young adults with influenza were 37 times higher in the autumn of 2009—when the H1N1 strain was predominant—than for the same period in the previous year, the latest figures for hospitals in England show.

Speaking at a briefing to reflect on the lessons learnt from the H1N1 outbreak, one year after it first emerged in Mexico, Peter Openshaw, director of the Centre for Respiratory Infection at the National Heart and Lung Institute, Imperial College London, reported that adults aged 17 to 39 years with flu accounted for 6253 hospital bed days during October to December 2009, compared with 169 in the same period in 2008.

“These figures show the remarkable impact of the H1N1 virus,” he said, adding that the pandemic behaved in a very different way from seasonal flu, which would …
A CASE OF FOREIGN BODY IN A BRONCHUS.
Authors: THOMAS A. CLAYTOR
Journal: JAMA (1905)

<h3>Patient.</h3> —On March 19, 1905, I was called to a neighboring town to see T. G., a boy, aged 5 years and 7 months, who, for the past twelve days, had suffered with a bad cough and an irregular fever, ranging from 99 in the morning to 104 in the evening. He seemed cheerful and free from pain, but there was a frequent cough, consisting of two or three expiratory efforts. The temperature was 105; the pulse, 120, and the respirations, 60 a minute. <h3>Examination.</h3> —The expansion was markedly diminished on the right side of the chest. The voice was too weak to allow of the detection of any differences in tactile fremitus, but there was certainly no increase over any area. Percussion showed a slightly higher pitch over the entire right lung, but only one small area of dullness extending from the angle of the scapula down to the
Infantile Fibrosarcoma: Management Based on the European Experience
Authors: Daniel Orbach, Annie Rey, Giovanni Cecchetto, Odile Oberlin, Michela Casanova, Estelle Thebaud, Marcelo Scopinaro, Gianni Bisogno, Modesto Carli, Andrea Ferrari
Journal: Journal of Clinical Oncology (2009)

Purpose To retrospectively analyze the clinical features and results of treatment in 56 infants with fibrosarcoma enrolled onto cooperative European protocols between 1979 and 2005 and treated with a combination of surgery and chemotherapy. Patients and Methods We performed a retrospective case review of infants under the age of 2 years with fibrosarcoma treated between 1979 and 2005 in six European studies. Patients were staged according to the Intergroup Rhabdomyosarcoma Staging System international classification as a function of the type of initial surgery and the extent of disease and were treated with surgery and chemotherapy. Survival was calculated using the Kaplan-Meier method. Results Primary tumor site was the limbs in 66% of patients; median tumor diameter was more than 5 cm in 63% of patients; and postoperative staging was as follows: group I, 22%; group II, 27%; group III, 47%; and group IV, 4%. Response rate to chemotherapy was 75%, and the specific response rate to vincristine-dactinomycin was 71%. Local control was obtained in 84% of patients. At the end of follow-up, 45% of survivors had been treated by surgery alone, 6% by chemotherapy alone, 46% by surgery and chemotherapy, and 2% by surgery, chemotherapy, and radiotherapy. The 5-year overall survival (OS) rate was 89%. The 5-year OS and event-free survival rates for localized patients were 89% and 81%, respectively. Conclusion Although complete resection is rarely feasible at diagnosis, conservative surgery remains the mainstay treatment for infantile fibrosarcoma. An alkylating agent–free and anthracycline-free regimen is usually effective and should be chosen as first-line chemotherapy for inoperable tumors. Overall prognosis is good, but progression or relapse, mainly local, remains possible.
Symmetrical Cervical Muscle Uptake of Ga-67 in Lyme Disease
Authors: WILLIAM DENISON, RACHEL POWSNER
Journal: Clinical Nuclear Medicine (1995)

An unfortunate dermal exposure to an Ixodes tick infected with the spirochete Borrelia burgdorferi causes the multifaceted Lyme disease. Patients with Lyme disease have dermatologic, arthritic, neurologic, and cardiac abnormalities. Also, symptoms secondary to musculoskeletal inflammation may be present. A case of a 28-year-old man who presented with flu-like symptoms and neck pain is presented. A Ga-67 scan revealed marked symmetric increased posterior cervical muscular uptake in the distribution of the splenius capitls and semispinalls muscles, which is most likely due to inflammation secondary to spirochete organisms within these tissues.
Price of Health Care Services
Authors: Mike Mitka
Journal: JAMA (2011)

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
The Use of SPECT in the Diagnosis of Epiphyseal Osteoid Osteoma
Authors: I P C MURRAY, M A ROSSLEIGH, H VAN DER WALL
Journal: Clinical Nuclear Medicine (1989)

An osteoid osteoma, which rarely occurs in an intraeplphyseal site, was identified by SPECT imaging in the proximal tibial epiphysis of a boy who had lower back pain, which had not been explained by extensive prior investigations.
Chronic Endothelin Receptor Antagonism Preserves Coronary Endothelial Function in Experimental Hypercholesterolemia
Authors: Patricia J. M. Best, Charles J. McKenna, David Hasdai, David R. Holmes, Amir Lerman
Journal: Circulation (1999)

Endothelin-1 (ET-1) is an endothelium-derived peptide that constricts coronary vessels through stimulation of the ET-A and ET-B receptors. Experimental porcine hypercholesterolemia is associated with impaired coronary endothelial function and elevated ET-1 concentrations. This study was designed to test the hypothesis that chronic endothelin receptor antagonism preserves coronary endothelial function in experimental hypercholesterolemia.Acetylcholine (10(-6) to 10(-4) mol/L) was serially infused into the left anterior descending coronary artery in pigs at baseline and after 12 weeks of a high-cholesterol diet. In the interim, the animals were randomized to 3 groups: Group 1 received no therapy, group 2 received 3 mg/kg per day RO 48-5695, a combined ET-A/ET-B receptor antagonist, and group 3 received 4 mg/kg per day ABT-627, a selective ET-A receptor antagonist. Percent change in coronary artery diameter, coronary blood flow, and coronary vascular resistance were calculated on the basis of quantitative coronary angiography and intracoronary Doppler. At 12 weeks, total cholesterol was significantly and similarly increased in all groups. Chronic endothelin receptor antagonism significantly increased coronary blood flow in response to acetylcholine at 12 weeks (group 1: -41.6%+/-10.7%, group 2: -4.7%+/-11.9%, group 3: 11.4%+/-7.4%).Chronic endothelin receptor antagonism preserves coronary endothelial function in experimental hypercholesterolemia. This study supports the role for ET-1 in the pathogenesis of endothelial function. Moreover, endothelin receptor antagonists may have a therapeutic role by maintaining coronary endothelial function in pathophysiological states.
Cap polyposis occurring in the postoperative course of pelvic surgery.
Authors: M Gehenot, J F Colombel, E Wolschies, P Quandalle, P Gower, M Lecomte-Houcke, H Van Kruiningen, A Cortot
Journal: Gut (1994)

The case is reported of a 42 year old woman who presented with the characteristic clinical, sigmoidoscopic, and histological features of cap polyposis occurring in the postoperative course of pelvic surgery. Pathogenesis of cap polyposis is unknown. In this patient, abnormal colonic motility was not a likely aetiological factor as suggested in previous cases. Despite some arguments favouring an infectious origin or participation, no specific viral or bacterial agent was identified. Cap polyposis remains a poorly recognised condition, which may be confused with inflammatory bowel disease.
<i>PEG10</i> Is a c-MYC Target Gene in Cancer Cells
Authors: Chi-Ming Li, Adam A. Margolin, Martha Salas, Lorenzo Memeo, Mahesh Mansukhani, Hanina Hibshoosh, Matthias Szabolcs, Apostolos Klinakis, Benjamin Tycko
Journal: Cancer Research (2006)

Abstract The product of the imprinted gene paternally expressed gene-10 (PEG10) has been reported to support proliferation in hepatocellular carcinomas, but how this gene is regulated has been an open question. We find that MYC knockdown by RNA interference suppresses PEG10 expression in Panc1 pancreatic carcinoma and HepG2 hepatocellular carcinoma cells and that knockdown of PEG10 inhibits the proliferation of Panc1, HepG2, and Hep3B cells. Conversely, PEG10 was up-regulated by inducing c-MYC expression in a B-lymphocyte cell line. Chromatin immunoprecipitation from Panc1 cells showed c-MYC bound to an E-box-containing region in the PEG10 first intron and site-directed mutagenesis showed that the most proximal E-box is essential for promoter activity. In a mouse mammary tumor virus (MMTV)-MYC transgenic mouse model of breast cancer, most but not all of the mammary carcinomas had strongly increased Peg10 mRNA compared with normal mammary gland. By immunohistochemistry, normal human breast and prostate epithelium was negative for the major isoform [reading frame-1 (RF1)] of PEG10 protein, but this cytoplasmic protein was strongly expressed in a subset of breast carcinomas in situ and invasive ductal carcinomas (∼30%) and in a similar percentage of prostate cancers. As in the mouse model, we found positive, but not absolute, correlations between PEG10 and c-MYC in tissue arrays containing 161 human breast cancers (P &amp;lt; 0.002) and 30 prostate cancers (P = 0.014). Immunostaining of human placenta showed PEG10 and c-MYC proteins coexpressed in proliferating cytotrophoblast and coordinately lost in postmitotic syncytiotrophoblast. These findings link cancer genetics and epigenetics by showing that a classic proto-oncogene, MYC, acts directly upstream of a proliferation-positive imprinted gene, PEG10. (Cancer Res 2006; 66(2): 665-72)
Tobacco: Promotion and Smoking-Reply
Authors: John P. Pierce
Journal: JAMA (1992)

<h3>In Reply.</h3> —Mr Males takes issue with two of the three articles<sup>1,2</sup>that addressed the effect of tobacco company advertising on the probability of minors starting to smoke. He argues, incorrectly, that our data indicate that the rate of initiation of smoking did not increase during the recent period of heavy advertising with the new tobacco campaign. He implies that without such evidence our findings will later prove to be overstated. The key point of all three articles<sup>1-3</sup>in<i>JAMA</i>was that the effectiveness of tobacco advertising would slow the rate of decline in the uptake of smoking. Indeed, a number of studies indicates that the decline in smoking initiation has slowed significantly in recent years.<sup>4</sup>However, identification of a change in the rate of initiation in smoking from a tobacco industry campaign such as "Joe Smooth" probably will not be an immediate phenomenon. Nobody expects that
Novel Molecular Mechanism Involving α<sub>1D</sub>(Cav1.3) L-Type Calcium Channel in Autoimmune-Associated Sinus Bradycardia
Authors: Yongxia Qu, Ghayath Baroudi, Yuankun Yue, Mohamed Boutjdir
Journal: Circulation (2005)

Congenital heart block (CHB) is an autoimmune disease that affects fetuses/infants born to mothers with anti-Ro/La antibodies (positive IgG). Although the hallmark of CHB is complete atrioventricular block, sinus bradycardia has been reported recently in animal models of CHB. Interestingly, knockout of the neuroendocrine alpha1D Ca channel in mice results in significant sinus bradycardia and atrioventricular block, a phenotype reminiscent to that seen in CHB. Here, we tested the hypothesis that the alpha1D Ca channel is a novel target for positive IgG.Reverse transcription-polymerase chain reaction, confocal indirect immunostaining, and Western blot data established the expression of the alpha1D Ca channel in the human fetal heart. The effect of positive IgG on alpha1D Ca current (I(Ca-L)) was characterized in heterologous expression systems (tsA201 cells and Xenopus oocytes) because of the unavailability of alpha1D-specific modulators. alpha1D I(Ca-L) activated at negative potentials (between -60 and -50 mV). Positive IgG inhibited alpha1D I(Ca-L) in both expression systems. This inhibition was rescued by a Ca channel activator, Bay K8644. No effect on alpha1D I(Ca-L) was observed with negative IgG and denatured positive IgG. Western blot data showed that positive IgG binds directly to alpha1D Ca channel protein.The data are the first to demonstrate (1) expression of the alpha1D Ca channel in human fetal heart, (2) inhibition of alpha1D I(Ca-L) by positive IgG, and (3) direct cross-reactivity of positive IgG with the alpha1D Ca channel protein. Given that alpha1D I(Ca-L) activates at voltages within the pacemaker's diastolic depolarization, inhibition of alpha1D I(Ca-L) in part may account for autoimmune-associated sinus bradycardia. In addition, Bay K8644 rescue of alpha1D I(Ca-L) inhibition opens new directions in the development of pharmacotherapeutic approaches in the management of CHB.
The Chronically Ischemic Lower Limb
Authors: Irwin J. Schatz
Journal: JAMA (1966)

Proper advice to the patient with symptomatic arterial insufficiency of the leg due to atherosclerosis depends upon a thorough understanding of the natural history of this disease and adequate knowledge of those therapeutic maneuvers which are likely to improve its course. Prior to making specific recommendations for therapy, however, the physician first must determine whether there has been significant disruption of the patient's personality, his job, and his daily activity. Only after this judgment is made can treatment most appropriate for the particular patient's needs be applied. <h3>Natural History.—</h3> Before reviewing the available methods of therapy, several brief generalizations summarizing current knowledge of the natural history of peripheral atherosclerosis may be pertinent.<sup>1</sup> Significant coronary and cerebrovascular arterial disease usually is present in patients with intermittent claudication. The prognosis for life in this group is, in great part, determined by these lesions and consequently is considerably worse than that for
HCCS1-armed, quadruple-regulated oncolytic adenovirus specific for liver cancer as a cancer targeting gene-viro-therapy strategy
Authors: Hai-Neng Xu, Wei-Dan Huang, Ying Cai, Miao Ding, Jin-Fa Gu, Na Wei, Lan-Ying Sun, Xin Cao, Hua-Guang Li, Kang-Jian Zhang, Xin-Ran Liu, Xin-Yuan Liu
Journal: Molecular Cancer (2011)

Abstract Background In previously published studies, oncolytic adenovirus-mediated gene therapy has produced good results in targeting cancer cells. However, safety and efficacy, the two most important aspects in cancer therapy, remain serious challenges. The specific expression or deletion of replication related genes in an adenovirus has been frequently utilized to regulate the cancer cell specificity of a virus. Accordingly, in this study, we deleted 24 bp in E1A (bp924-bp947) and the entirety of E1B, including those genes encoding E1B 55kDa and E1B19kDa. We used the survivin promoter (SP) to control E1A in order to construct a new adenovirus vector named Ad.SP.E1A(Δ24).ΔE1B (briefly Ad.SPDD). HCCS1 (hepatocellular carcinoma suppressor 1) is a novel tumor suppressor gene that is able to specifically induce apoptosis in cancer cells. The expression cassette AFP-HCCS1-WPRE-SV40 was inserted into Ad.SPDD to form Ad.SPDD-HCCS1, enabling us to improve the safety and efficacy of oncolytic-mediated gene therapy for liver cancer. Results Ad.SPDD showed a decreased viral yield and less toxicity in normal cells but enhanced toxicity in liver cancer cells, compared with the cancer-specific adenovirus ZD55 (E1B55K deletion). Ad.SPDD-HCCS1 exhibited a potent anti-liver-cancer ability and decreased toxicity in vitro. Ad.SPDD-HCCS1 also showed a measurable capacity to inhibit Huh-7 xenograft tumor growth on nude mice. The underlying mechanism of Ad.SPDD-HCCS1-induced liver cancer cell death was found to be via the mitochondrial apoptosis pathway. Conclusions These results demonstrate that Ad.SPDD-HCCS1 was able to elicit reduced toxicity and enhanced efficacy both in vitro and in vivo compared to a previously constructed oncolytic adenovirus. Ad.SPDD-HCCS1 could be a promising candidate for liver cancer therapy.
CD8+ T Cells Mediate CD40-independent Maturation of Dendritic Cells In Vivo
Authors: Christiane Ruedl, Manfred Kopf, Martin F. Bachmann
Journal: The Journal of Experimental Medicine (1999)

Induction of cytotoxic T lymphocyte (CTL) responses against minor histocompatibility antigens is dependent upon the presence of T cell help and requires the interaction of CD40 on dendritic cells (DCs) with CD40 ligand on activated T helper cells (Th). This study demonstrates that CD40 is neither involved in Th-dependent nor Th-independent antiviral CTL responses. Moreover, the data show that DC maturation occurs in vivo after viral infection in the absence of CD40 and Th. This maturation did not require viral infection of DCs but was mediated by peptide-specific CD8+ T cells. Surprisingly, naive CD8+ T cells were able to trigger DC maturation within 24 h after activation in vivo and in vitro. Moreover, peptide-activated CD8+ T cells were able to induce maturation in trans, as DCs that failed to present the relevant antigen in vivo also underwent maturation. Upon isolation, the in vivo–stimulated DCs were able to convert a classically Th-dependent CTL response (anti-HY) into a Th-independent response in vitro. Thus, antiviral CD8+ T cells are sufficient for the maturation of DCs in the absence of CD40.
Abstract 1029: BB a novel Bim isoform upregulated in acute lymphoblastic leukemia after glucocorticoid monotherapy confers a novel apoptosis regulation mechanism
Authors: Alexander Trockenbacher, Muhammad Mansha, Christian Ploner, Reinhard Kofler
Journal: Cancer Research (2010)

Abstract Glucocorticoids (GCs) are fundamental components of most chemotherapies employed against lymphoid malignancies because they cause apoptosis and cell cycle arrest. In this study we investigate the possible role of a novel splice variant of human BCL2L11/Bim, termed BB, for GC-induced apoptosis. First evidence for BB was obtained by Affymetrix-based whole genome comparative expression profiling, where a corresponding probe set was found to be induced in 8 of the 13 ALL children and 1 adult during systemic GC monotherapy (Schmidt et al., 2006). The postulated BB mRNA consists of the 5’ portion of Bim (up to and including the BH3-containing exon 8) and the 3’ portion of Bam, a cDNA originally discovered in a multiple myeloma cDNA library (Claudio et al., 2002). Thus, it encodes a putative protein consisting of the N-terminal region of Bim (including its BH3 domain) and 40 C-terminal amino acids derived from Bam and not present in any known Bim transcript. BB and Bim proteins have similar molecular masses and could not be distinguished by conventional Western technology when probed by α-Bim antibody as most α-Bim antibodies recognize the N-terminal region which is common to both isoforms. RT-PCR data and protein analyses carried out by using α-Bam antibody (that recognizes the Bam specific C-terminal region) on GC-treated CEM-C7H2 cells supported the existence of the postulated BB mRNA and protein. Subcellular localization analysis of BB suggested that BB may be directed to mitochondria, ascribed probably to its BH3-domain interaction with other BCL2 proteins and not by its unique C-terminus which in contrast to the Bim C-terminus doesn't localize to mitochondria. The functional analyses with conditional overexpression in ALL in vitro model revealed that overexpressed BB is a killer protein with potency similar to that of Bim and thus may contribute to the anti-leukemic effects of GCs and perhaps other apoptotic responses. 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 1029.