tbuckley/cabot-search huggingface dataset:
Adult hepatitis B vaccination using a novel triple antigen recombinant vaccine
Authors: Michael D. Young, David L. Schneider, Arie J. Zuckerman, Wei Du, Brian Dickson, Willis C. Maddrey
Journal: Hepatology (2001)

Present hepatitis B vaccines use multidose prolonged regimens, which even healthcare workers at risk do not always complete. Moreover, when vaccination is completed there remain some who fail to achieve adequate protection. The protection of adults at risk could be improved if there were a more potent vaccine and/or a shorter vaccination regimen available. Vaccine–naive adults were randomized to vaccination with either Engerix–B (SmithKline Biologicals, Rixensart, Belgium) or a novel triple antigen (S, pre–S1, and pre–S2) recombinant vaccine (Hepacare; Medeva Pharma Plc, Speke, UK). The primary efficacy parameter was the degree of seroprotection 6 or 7 months (26 ± 2 weeks) after beginning vaccination. A total of 304 adults entered the study. Of these, 16 failed to complete the study (9 on Hepacare and 7 on Engerix–B). With the Engerix–B standard (0, 1, 6) regimen, 88% of subjects were protected by month 7, whereas with the triple antigen vaccine a 2–dose regimen (0, 1) provided equivalent protection (91%) within 6 months and a 3–dose (0, 1, 6) regimen was significantly superior (98% seroprotected by 7 months after starting vaccination P &lt; .001). With adults at risk for a suboptimal response ( i.e. , older adults, the obese, men, and smokers) the triple antigen vaccine produced a greater degree of protection. The vaccines had similar safety profiles. Both vaccines were well tolerated. In healthy normal adults, a triple antigen hepatitis B vaccine containing S and pre–S antigens produced an enhanced immunologic response and was as effective as a 2– and 3–dose regimen.
Strength-duration and probability of success curves for defibrillation with biphasic waveforms.
Authors: S A Feeser, A S Tang, K M Kavanagh, D L Rollins, W M Smith, P D Wolf, R E Ideker
Journal: Circulation (1990)

Certain biphasic waveforms require less energy to defibrillate than do monophasic pulses of equal duration, although the mechanisms of this increased effectiveness remain unclear. This study used strength-duration and percent success curves for defibrillation with monophasic and biphasic truncated exponential waveforms to explore these mechanisms. In part 1, defibrillation thresholds were determined for both high- and low-tilt waveforms. The monophasic pulses tested ranged in duration from 1.0 to 20.0 msec, and the biphasic waveforms had first phases of either 3.5 or 7.0 msec and second phases ranging from 1.0 to 20.0 msec. In part 2, defibrillation percent success curves were constructed for 6.0 msec/6.0 msec biphasic waveforms with a constant phase-one amplitude and with phase-two amplitudes of approximately 21%, 62%, 94%, and 141% of phase one. This study shows that if the first phase of a biphasic waveform is held constant and the second phase is increased in either duration or amplitude, defibrillation efficacy first improves, then declines, and then again improves. For pulse durations of at least 14 msec, the second-phase defibrillation threshold voltage of a high-tilt biphasic waveform is higher than that of a monophasic pulse equal in duration to the biphasic second phase (p less than 0.05), indicating that the previously proposed hypothesis of stimulation by the second phase is not the sole mechanism of biphasic defibrillation. These facts indicate the importance of the degree of tilt for the defibrillation efficacy of biphasic waveforms and suggest at least two mechanisms exist for defibrillation with these waveforms, one that is more effective for smaller second phases and another that becomes more effective as the second phase is increased.
Relationship between Serum IgE Concentration and Occurrence of Immediate Skin Test Reactions and Allergic Disorders in Young People
Authors: Tari Haahela, Ilpo Suoniemi, Ilmari Jaakonmäki, Fred Björksten
Journal: Allergy (1982)

We studied serum IgE concentration by the PRIST® method in 157 adolescents (71 boys) aged 15–17 years. This group was randomly drawn from a larger unselected population of 708 young people. The geometric mean IgE for the 157 subjects was 37.6 U/ml. After careful exclusion 77 subjects without any signs or symptoms of atopy were found. The mean IgE for them was 16.6U/ml. Nineteen per cent of the population had an IgE. concentration higher than 160 /ml and 30% had a value below 20 U/ml. Positive skin test reactions were strongly associated with increased IgE level, byt the effect of bronchial wheezing was insignificant. We conclude that IgE concentrations above 160 U/ml during adolescence suggest atopy and correlate with positive skin test reactivity and /or clinical symptoms. An IgE value below 20U/ml almost certainly excludes the possibility of positive skin reactions and somewhat less certainly the possibility that symptoms are due to atopy.
Pacemakers and End-of-Life Decisions
Authors: Rachel Lampert
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
An Association Study of <i>CASQ1</i> Gene Polymorphisms and Heat Stroke
Authors: Ying Li, Yu Wang, Lin Ma
Journal: Genomics Proteomics & Bioinformatics (2014)

Although molecular mechanisms of heat stroke under physiological and pathological conditions have not yet been elucidated, a novel disease-associated gene encoding a calcium-binding protein, calsequestrin-1 (CASQ1), was suggested relevant based on results from a transgenic murine model. Here, we show the association between single nucleotide polymorphisms (SNPs) of CASQ1 and physiological parameters for heat stroke from a study involving 150 patients. Pooled DNA from heat stroke patients were subjected to sequencing and 3 SNPs were identified. Genotypes were assigned for all patients according to g. 175A>G, one SNP which leads to a nonsynonymous substitution (N59D) in the first exon of human CASQ1 gene. We analyzed the genotypic data with a linear model based on significance scores between SNP (175A>G) and heat stroke parameters. As a result, we found a significant association between SNP A175G and heat stroke (P<0.05). Further bioinformatics analysis of the 1-Mb flanking sequence revealed the presence of two genes that encode DDB1 and CUL4 associated factor 8 (DCAF8), and peroxisomal biogenesis factor 19 (PEX19), respectively, which might be functionally related to CASQ1. Our results showed that the blood calcium of patients with allele D increased significantly, compared to patients with allele N (P<0.05), which may result from the decreased calcium in muscle, suggesting that N59D in CASQ1 might account for the dysfunction of CASQ1 in calcium regulation during heat stroke.
835. Inhibition of Hepatic SPARC (Secreted Protein Acidic and Rich in Cysteine) Expression for the Treatment of Experimental Cirrhosis
Authors: Alejandra M. Camino, Federico Prada, Osvaldo Podhajcer, Marcelo O. Silva, Guillermo D. Mazzolini
Journal: Molecular Therapy (2006)

Introduction: SPARC is a 42-kDa matricellular glycoprotein involved in many biological process including cell adhesion, differentiation and proliferation. SPARC is also expressed by activated hepatic stellate cells suggesting its involvement in liver fibrogenesis. Aim: to determine whether liver gene delivery of a SPARC antisense mRNA (AdasSPARC) would prevent hepatic fibrosis in an animal model. M&M: Intraperitoneal injection of thioacetamide (TAA) was used to induce cirrhosis in Sprague-Dawley rats. Animals received injections of a recombinant adenovirus encoding a SPARC antisense mRNA (AdasSPARC) or a control adenovirus encoding b-galactosidase gene (Adbgal) via the tail vein at the beginning of TAA administration. At day 7 the animals received a second dose directly into the liver by laparotomy. Antifibrotic effects of SPARC inhibition were assessed by histological examination, quantification of extracellular matrix deposition and activation of hepatic stellate cells (HSC). Results: The percentage of fibrosis area in the liver by image analysis of Sirius red staining was decreased in AdasSPARC treated animals (11%± 0.04%) in comparison with animals treated with Adbgal or saline (27% ± 0.15% and 28%± 0.16 %, respectively). Quantification of hepatic hydroxyproline confirmed that a SPARC antisense mRNA expression in the liver attenuated collagen deposition. In the livers of rats treated with saline or Adbgal, no significant prevention in the fibrosis score was observed (F3–F4). Contrarily, only slight to moderate fibrosis was observed in the animals that received AdasSPARC (F1-F2). The total Knodell score of saline and Adbgal treated rats was greater than those of AdasSPARC treated rats (13/22, 10/22 and 6/22, respectively). By immunohistochemistry analysis, SPARC protein was highly expressed on liver tissue from control rats and significant inhibition was observed in AdasSPARC treated animals. The number of cells positive for a-smooth muscle actin was significantly reduced in animals after the administration of AdasSPARC. Conclusions: Taken together, our results provide in vivo evidence that adenovirus-mediated gene transfer of a SPARC antisense mRNA in the liver ameliorates fibrosis and necroinflammatory activity induced by TAA.
Hormonal Effects on Cell Membrane Function.
Authors: Rachmiel Levine
Journal: Annals of Internal Medicine (1973)

Meeting Abstracts1 May 1973Hormonal Effects on Cell Membrane Function.Rachmiel Levine, M.D., F.A.C.P.Rachmiel Levine, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-78-5-813_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe cell membrane regulates substrate intake, waste excretion, mineral balance, gas exchange, and reception and translation of chemical and physical stimuli. The membrane is a precisely fashioned supramolecular assembly of phospholipids, simple proteins, glycoproteins, and lipoproteins. Enzymes and transport proteins form part of its structure. Specific molecules at the surface serve as receptors for a variety of hormones, especially those with peptide- or amino acid-derivative structure. The interaction of a hormone with its membrane receptor may modify rates and direction of substrate transport and give rise to "secondary messages" that modulate other cell functions.Present concepts will be reviewed, with... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Duarte, California PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1973Volume 78, Issue 5Page: 813-813KeywordsCell membranesEnzymesExcretionGlycoproteinsHormonesLipoproteinsMembrane proteinsPeptide hormonesPhospholipidsProtein structure Issue Published: 1 May 1973 PDF DownloadLoading ...
Women need better information on routine mammography: Information on expected mortality reduction from attending screening must be correct
Authors: R. G. Blanks
Journal: BMJ (2003)

Editor—Thornton et al say that claims for the reduction in relative risk of death from breast cancer among women who are screened have ranged from 63% to 6%.1 This is crucial information for women considering attending. Unfortunately the lower limit, attributed to our paper in the BMJ in 2000,2 is no such estimate. The 6% refers to the reduction seen in death rates from breast cancer for invited women (including those screened and non-attenders) in 1998, from a programme that started between 1988 and 1995.

For reasons we explained in great detail in our paper (including the fact that many deaths in the 1990s will have been women with a diagnosis of breast cancer before any invitation to screening), this is most likely to estimate the beginnings of an effect—not the full effect. It is therefore inaccurate and extremely unhelpful to quote this figure to women as an estimated relative risk reduction from attending screening—it is not.
Deficiency of the Housekeeping Gene Hypoxanthine–Guanine Phosphoribosyltransferase (HPRT) Dysregulates Neurogenesis
Authors: Ghiabe-Henri Guibinga, Stephen Hsu, Theodore Friedmann
Journal: Molecular Therapy (2009)

Neuronal transcription factors play vital roles in the specification and development of neurons, including dopaminergic (DA) neurons. Mutations in the gene encoding the purine biosynthetic enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT) cause the resulting intractable and largely untreatable neurological impairment of Lesch-Nyhan disease (LND). The disorder is associated with a defect in basal ganglia DA pathways. The mechanisms connecting the purine metabolic defect and the central nervous system (CNS) phenotype are poorly understood but have been presumed to reflect a developmental defect of DA neurons. We have examined the effect of HPRT deficiency on the differentiation of neurons in the well-established human (NT2) embryonic carcinoma neurogenesis model. We have used a retrovirus expressing a small hairpin RNA (shRNA) to knock down HPRT gene expression and have examined the expression of a number of transcription factors essential for neuronal differentiation and marker genes involved in DA biosynthetic pathway. HPRT-deficient NT2 cells demonstrate aberrant expression of several transcription factors and DA markers. Although differentiated HPRT-deficient neurons also demonstrate a striking deficit in neurite outgrowth during differentiation, resulting neurons demonstrate wild-type electrophysiological properties. These results represent direct experimental evidence for aberrant neurogenesis in HPRT deficiency and suggest developmental roles for other housekeeping genes in neurodevelopmental disease.
Hypomorphic mutations in syndromic encephalocele genes are associated with Bardet-Biedl syndrome
Authors: Carmen C Leitch, Norann A Zaghloul, Erica E Davis, Corinne Stoetzel, Anna Diaz-Font, Suzanne Rix, Majid Alfadhel, Richard Alan Lewis, Wafaa Eyaid, Eyal Banin, Helene Dollfus, Philip L Beales, Jose L Badano, Nicholas Katsanis
Journal: Nature Genetics (2008)
Case 3-1976
Authors: Richard C. Cabot, Robert E. Scully, James J. Galdabini, Betty U. McNeely, Adolph M. Hutter, Cary W. Akins
Journal: New England Journal of Medicine (1976)

Presentation of Case First admission. A 15-year-old boy was admitted to the hospital because of the recent finding of a heart murmur.One month before admission, while playing basketball, he was struck in the chest by the knee of an opposing player. He was taken to another hospital, where an x-ray film of the chest was reported to be normal. On the following day he was seen at this hospital. Physical examination was negative; the blood pressure was 110/70 mm Hg, and no cardiac abnormality was found. He complained repeatedly of soreness in the anterior portion of the chest . . .
Glycine substitution mutations by different amino acids at the same codon in <i>COL7A1</i> cause different modes of dystrophic epidermolysis bullosa inheritance
Authors: D. Sawamura, Y. Mochitomi, T. Kanzaki, H. Nakamura, H. Shimizu
Journal: British Journal of Dermatology (2006)

Journal Article Glycine substitution mutations by different amino acids at the same codon in COL7A1 cause different modes of dystrophic epidermolysis bullosa inheritance Get access D. Sawamura, D. Sawamura Department of Dermatology, Hokkaido University Graduate School of Medicine, North 15 West 7, Kita‐ku, Sapporo 060‐8638, Japan *Department of Dermatology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan E‐mail: smartdai@med.hokudai.ac.jp Search for other works by this author on: Oxford Academic Google Scholar Y. Mochitomi, Y. Mochitomi Department of Dermatology, Hokkaido University Graduate School of Medicine, North 15 West 7, Kita‐ku, Sapporo 060‐8638, Japan *Department of Dermatology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan E‐mail: smartdai@med.hokudai.ac.jp Search for other works by this author on: Oxford Academic Google Scholar T. Kanzaki, T. Kanzaki Department of Dermatology, Hokkaido University Graduate School of Medicine, North 15 West 7, Kita‐ku, Sapporo 060‐8638, Japan *Department of Dermatology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan E‐mail: smartdai@med.hokudai.ac.jp Search for other works by this author on: Oxford Academic Google Scholar H. Nakamura, H. Nakamura Department of Dermatology, Hokkaido University Graduate School of Medicine, North 15 West 7, Kita‐ku, Sapporo 060‐8638, Japan *Department of Dermatology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan E‐mail: smartdai@med.hokudai.ac.jp Search for other works by this author on: Oxford Academic Google Scholar H. Shimizu H. Shimizu Department of Dermatology, Hokkaido University Graduate School of Medicine, North 15 West 7, Kita‐ku, Sapporo 060‐8638, Japan *Department of Dermatology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan E‐mail: smartdai@med.hokudai.ac.jp Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 155, Issue 4, 1 October 2006, Pages 834–837, https://doi.org/10.1111/j.1365-2133.2006.07388.x Published: 01 October 2006 Article history Accepted: 16 March 2006 Published: 01 October 2006
The plasma kinetics of hydroxyethyl starch 350/0.60: A potential new adjunct for centrifugal leucapheresis
Authors: John Milton Mishler
Journal: American Journal of Hematology (1979)

A modified species of hydroxyethyl starch (HES 350/0.60) possessing a Mw- of 350,000 daltons combined with a molar hydroxyethyl group substitution (MS) of 0.60 (60 hydroxyethyl groups.100 glucose residues) was clinically assessed in seven normal subjects to determine the influence of these chemical modifications on intravascular clearance kinetics concomitantly with effects on the suspension stability (ESR) of blood. Following a standardised intravenous dose (30 gm.m2 BSA), the concentration of HES 350/0.60 in serum fell to half its peak value in 11.8 +/- 1.3 (SD) hours, while the ESR remained elevated for up to 12 hours post-injection. By adopting a Mw- of 350,000 daltons, the critical molecular weight (Cmw) of this colloid was surpassed, while the critical concentration (Cc), below which the suspension stability of blood is not affected, was shown to range between 0.3 and 0.5 gm.dl-1. In comparison to the present species of HES (Mw- 450,000 daltons, MS: 0.70) utilised as a sedimenting agent duirng centrifugal leucapheresis, HES 350,000/0.60 appears to affect the ESR in a similar manner, but is removed from the intravascular space approximately twice as rapidly. This more rapid clearance should be useful in avoiding cumulative build-up of HES in blood concomitant with reducing the total amount of intravascular H2O bound to this colloid, in normal and CML donors undergoing multiple cell collection procedures.
Normal Development of the Outflow Tract in the Rat
Authors: Jing Ya, Maurice J. B. van den Hoff, Piet A. J. de Boer, Sabina Tesink-Taekema, Diego Franco, Antoon F. M. Moorman, Wouter H. Lamers
Journal: Circulation Research (1998)

Abstract —The outflow tract (OFT) provides the structural components forming the ventriculoarterial connection. The prevailing concept that this junction “rotates” to acquire its definitive topography also requires a concept of “counterrotation” and is difficult to reconcile with cell-marking studies. Rats between 10 embryonic days (EDs) and 2 postnatal days were stained immunohistochemically and by in situ hybridization. DNA replication was determined by incorporation of bromodeoxyuridine and apoptosis by the annexin V binding and terminal deoxynucleotidyl transferase–mediated dUTP-X nick end labeling (TUNEL) assays. Starting at ED12, cardiomyocytes in the distal (truncal) part of the OFT begin to shed their myocardial phenotype without proceeding into apoptosis, suggesting transdifferentiation. Myocardial regression is most pronounced on the dextroposterior side and continues until after birth, as revealed by the disappearance of the myocardial cuff surrounding the coronary roots and semilunar sinuses and by the establishment of fibrous continuity between mitral and aortic semilunar valves. Fusion of the endocardial ridges of the truncus on late ED13 is accompanied by the organization of α-smooth muscle actin–and nonmuscle myosin heavy chain–positive myofibroblasts into a central whorl and the appearance of the semilunar valve anlagen at their definitive topographical position within the proximal portion of the truncus. After fusion of the proximal (conal) portion of the endocardial ridges, many of the resident myofibroblasts undergo apoptosis and are replaced by cardiomyocytes. The distal myocardial boundary of the OFT is not a stable landmark but moves proximally over the spiraling course of the aortic and pulmonary routes, so that the semilunar valves develop at their definitive topographic position. After septation, the distal boundary of the OFT continues to regress, particularly in its subaortic portion. The myocardializing conus septum, on the other hand, becomes largely incorporated into the right ventricle. These opposite developments account for the pronounced asymmetry of the subaortic and subpulmonary outlets in the formed heart.