tbuckley/cabot-search huggingface dataset:
Arrhythmogenic right ventricular dysplasia type 1 and mutations in transforming growth factor ?3 gene regulatory regions: a breakthrough?
Authors: S NATTEL, J SCHOTT
Journal: Cardiovascular Research (2004)

See article by Beffagna et al. (pages 366–373) in this issue .

Arrhythmogenic right ventricular dysplasia (ARVD) is the second most common cause of sudden unexpected death in young adults [1], responsible for ∼20% of sudden deaths in this population [2]. Subsequent to the description of the first case in 1961 [3], great progress has been made in the diagnosis, evaluation and management of the condition. The hallmark of ARVD is right ventricular atrophy with fibro-fatty infiltration. There is approximately threefold male predominance, and typical abnormalities include signs of right ventricular thinning and dysfunction and fragmented, low-amplitude late-QRS potentials in the right precordial leads identified on standard (“epsilon waves”) or signal-averaged electrocardiograms [2]. Familial occurrence is common, and in ∼30% of cases evidence has been found for autosomal-dominant inheritance with variable penetrance [4].

A variety of chromosomal locations have been identified in various kindreds with the condition (for review, see Ref. [2]). Eight subtypes identified as ARVD1–8 have been recognized. The specific gene underlying ARVD has been identified for a small number of subtypes. ARVD2, with features perhaps more typical of a catecholamine-dependent ventricular tachyarrhythmia syndrome than of ARVD, is associated with a mutation in ryanodine receptor-2 [5]. … 

*Corresponding author. Tel.: +1 514 376 3330; fax: +1 514 376 1355. Email address: stanley.nattel{at}icm-mhi.org
THE EARLY RECOGNITION AND TREATMENT OF CANCER OF THE STOMACH
Authors: E. Spriggs
Journal: BMJ (1928)

Wom11enll dial pai5ters whlo wzere suffering from-l the effects of radiation.One of the wvomiieni hadl lost a sister, aged 21, from necrosis of the jawbhone, wlhile anotlher had lost her * A contribution (abbrevi.ated)to the discussion, on July 20th, at the International Congress on Cancrx.
Continuing mortality and morbidity from smallpox vaccination.
Authors: G C Du Mont, R C Beach
Journal: BMJ (1979)

Three cases of cross-infection after smallpox vaccination are described, in two of which the outcome was fatal. Probably all occurred because simple precautions were not observed at the time of vaccination--for example, exclusion of contraindications and warnings about risks. If those countries still requiring evidence of vaccination for entry were to abolish this rule, however, the risk of cross-infection could be eliminated. Vaccinating a person with contraindications is justified only when exposure to smallpox has occurred.
Low Exposure To Inhaled Formaldehyde: Effect On Allergen Bronchial Response In Asthmatics Sensitized To Mite
Authors: A. Casset, C. Marchand, A. Purohit, S. Le Calve, C. Donnay, P. Meyer, G. Pauli, F. De Blay
Journal: Journal of Allergy and Clinical Immunology (2006)
Mechanism of secretion of biliary lipids. I. Role of bile canalicular and microsomal membranes in the synthesis and transport of biliary lecithin and cholesterol.
Authors: D H Gregory, Z R Vlahcevic, P Schatzki, L Swell
Journal: Journal of Clinical Investigation (1975)

The role of bile canalicular and microsomal membranes in the synthesis and transport of biliary lipids was investigated by using the isolated perfused rat liver model. Labeled lecithin precursors ((3H)-palmitic acid, (14C)linoleic acid, (3H)choline, and 32PO4) and a cholesterol precursor ((3H)mevalonic acid) were administered with and without sodium taurocholate. The incorporation pattern of these labeled precursors into linoleyl and arachidonyl lecithins and cholesterol fractions of microsomes, bile canaliculi, and bile were examined at 30-min intervals up to 90 min. Marker enzymes and electron microscopy indicated that isolated subfractions of plasma membranes were enriched with bile canaliculi (less than 10 percent microsomal contamination). Taurocholate significantly stimulated the incorporation of 32PO4, (3H)choline, (3H)palmitic acid, and (14C)linoleic acid into linoleyl and arachidonyl lecithin with parallel incorporation curves for microsomal and bile canalicular membranes throughout the 90-min study period. During the 30-60-min period, however, these same lecithin fractions in bile significantly exceeded the specific activity of the membrane lecithins. The enzyme CDP-choline diglyceride transferase was virtually absent from canaliculi relative to microsomes, indicating that canaliculi lack the capacity for de novo lecithin synthesis. Incorporation of (3H)mevalonic acid into membranous and biliary cholesterol followed a pattern similar to that for lecithin. These data provide evidence that (a) biliary lecithin and cholesterol are derived from a microsomal subpool regulated by the flux of enterohepatic bile acids, (b) the role of the bile canalicular membranes with respect to biliary lipids is primarily transport rather than synthesis, and (c) lecithin and cholesterol are transported together from microsomes to bile. The findings are consistent with the existence of a cytoplasmic lipid complex within the hepatocyte which is actively involved in the intermembrane transport of biliary lipid.
Coronary Artery Calcium in Acute Coronary Syndromes
Authors: Axel Schmermund, Dietrich Baumgart, Günter Görge, Rainer Seibel, Dietrich Grönemeyer, Junbo Ge, Michael Haude, John Rumberger, Raimund Erbel
Journal: Circulation (1997)

Background Quantification of coronary artery calcified plaques by electron-beam CT (EBCT) may predict cardiovascular events. However, whereas advanced coronary atherosclerotic plaques can be identified, mildly stenotic lipid-rich (soft) plaques may be difficult to detect. The value of EBCT in a subgroup of patients has therefore been questioned. To investigate this, we evaluated patients with acute coronary syndromes by EBCT and compared the results with coronary angiography and, in patients with an indeterminate angiogram, intracoronary ultrasound (ICUS). Methods and Results EBCT was performed in 118 consecutive patients (57±11 years of age) with previous myocardial infarction (n=101) or unstable angina (n=17). A standard protocol requiring a CT density &gt;130 Hounsfield units in an area ≥1.03 mm 2 was used for the definition of coronary artery calcium. We found that 110 patients had moderate to severe coronary artery disease by coronary angiography, and 8 had either mildly stenotic plaques at a single site (4 patients, confirmed by ICUS) or nonatherosclerotic causes of the unstable coronary syndrome (4 patients). One hundred and five of the 110 patients (96%) with moderate to severe angiographic disease but only 1 of the 8 other patients (13%) had a positive EBCT. Patients with acute coronary syndromes and negative EBCTs were significantly younger than patients with positive EBCTs (46±12 versus 58±10 years, P &lt;.001), and a higher percentage was actively smoking (100% of the smokers versus 46%, P &lt;.05). Conclusions The vast majority of patients with acute coronary syndromes and at least moderate angiographic disease have identifiable coronary calcium by EBCT. Those patients with negative EBCTs have minimal or no atherosclerotic plaque formation. They are younger and tend to be active cigarette smokers.
Amenorrhea from Breast Cancer Therapy — Not a Matter of Dose
Authors: Sandra M. Swain, Jong-Hyeon Jeong, Norman Wolmark
Journal: New England Journal of Medicine (2010)

To the Editor: In our article on concurrent versus sequential administration of chemotherapy drugs for women with operable, node-positive, early-stage breast cancer (June 3 issue),1 we report that premenopausal women in whom amenorrhea developed as a consequence of receiving adjuvant chemotherapy had a superior outcome to those without amenorrhea. In response to questions regarding our data analyses, we have performed two additional analyses. One is a 12-month landmark Kaplan–Meier analysis to address the concern that our previous results may have been biased by the misclassification of women without amenorrhea who had a relapse or died before reaching 24 months of . . .
VDIPEN, a metalloproteinase-generated neoepitope, is induced and immunolocalized in articular cartilage during inflammatory arthritis.
Authors: I I Singer, D W Kawka, E K Bayne, S A Donatelli, J R Weidner, H R Williams, J M Ayala, R A Mumford, M W Lark, T T Glant
Journal: Journal of Clinical Investigation (1995)

The destruction of articular cartilage in immune inflammatory arthritic disease involves the proteolytic degradation of its extracellular matrix. The role of activated matrix metalloproteinases (MMPs) in the chondrodestructive process was studied by identifying a selective cleavage product of aggrecan in murine arthritis models initiated by immunization with either type II collagen or proteoglycan. We conducted semiquantitative immunocytochemical studies of VDIPEN341 using a monospecific polyclonal antibody requiring the free COOH group of the COOH-terminal Asn for epitope detection. This antibody recognizes the aggrecan G1 domain fragment generated by MMP [i.e., stromelysin (SLN) or gelatinase A] cleavage of aggrecan between Asn341-Phe342 but does not recognize intact aggrecan. VDIPEN was undetectable in normal mouse cartilage but was observed in the articular cartilage (AC) of mice with collagen-induced arthritis 10 d after immunization, without histological damage and clinical symptoms. This aggrecan neoepitope was colocalized with high levels of glycosaminoglycans (GAGs) in pericellular matrices of AC chondrocytes but was not seen at the articular surface at this early time. Digestion of normal (VDIPEN negative) mouse paw cryosections with SLN also produced heavy pericellular VDIPEN labeling. Computer-based image analysis showed that the amount of VDIPEN expression increased dramatically by 20 d (70% of the SLN maximum) and was correlated with GAG depletion. Both infiltration of inflammatory cells into the synovial cavity and early AC erosion were also very prominent at this time. Analysis of adjacent sections showed that both induction of VDIPEN and GAG depletion were strikingly codistributed within sites of articular cartilage damage. Similar results occurred in proteoglycan-induced arthritis, a more progressive and chronic model of inflammatory arthritis. These studies demonstrate for the first time the MMP-dependent catabolism of aggrecan at sites of chondrodestruction during inflammatory arthritis.
"SERUM DIAGNOSIS OF SYPHILIS"-Reply
Authors: Hideyo Noguchi
Journal: JAMA (1918)

[The foregoing communication was referred to Dr. Noguchi, who replies:] <h3>To the Editor:</h3> —In reply to the criticism of Dr. J. J. Seelman, who has expressed apprehension with regard to the reliability of the serodiagnostic procedure described by me inThe Journal, I wish to make the following statement: Dr. Seelman regards my proposed method as less accurate in its quantitative aspect than the Wassermann system because of the variation in complement in different human serums, but he apparently ignores the inherent source of error in the latter from the varying amounts of natural antisheep amboceptor present in various human serums. Now, whereas ninety out of a hundred serums contain a practically constant quantity of complement, and no hypercomplementary serum contains more than twice this average complement content, the amount of natural antisheep amboceptor varies from none to as many as twenty units or more. In the homohemolytic system only
The prevalence of abnormal hepatic biochemistry and hepatobiliary morbidity in a cohort of patients with inflammatory bowel disease
Authors: M. B. Davies, J. F. L. Cobbold, D. G. Walker, H. R. Williams, T. R. Orchard
Journal: Gut (2011)

<h3>Introduction</h3> There is a recognised association between Inflammatory Bowel Disease (IBD) and both abnormal hepatic biochemistry and hepatobiliary morbidity. Hepatic steatosis, primary sclerosing cholangitis (PSC), cholelithiasis and drug reactions have all been linked, but the nature of the association and risk factors are unclear. The aims of this study were: (1) to assess the prevalence of, and risk factors for abnormal biochemistry in a cohort of patients with IBD; (2) to determine the prevalence of hepatobiliary morbidity in those patients with abnormal liver function tests (LFTs). <h3>Methods</h3> Ethical approval was obtained to take demographic and clinical data retrospectively from the IBD database of a secondary/tertiary referral centre, entered prospectively from January 2006 to September 2009. IBD diagnosis was based on endoscopic, radiological and histological criteria and disease phenotyping was according to the Montreal classification. Abnormal hepatic biochemistry was defined as elevation above the laboratory upper limit of normal for ALT (&gt;40 IU/l) and/or ALP (&gt;130 IU/l) and/or Bilirubin (&gt;17 mmol/l) at time of entry into the database. Fishers Exact and Mann-Whitney U tests were used. <h3>Results</h3> Of 493 patients in the database, 370 (75%) had hepatic biochemistry available. Of these, the prevalence of abnormal hepatic biochemistry was 17.8% and 10.8% had abnormal ALT. African-Caribbean patients had a high prevalence of abnormal hepatic biochemistry (11/23, 48%, p=0.001), in contrast to South Asian patients (5/49, 10%, p=0.16) and White British patients (24/152, 15.8%, p=0.4). Overall, there was no association with age, sex, diagnosis (Crohn9s or Ulcerative Colitis), disease phenotype or use of Azathioprine or Infliximab. Hepatobiliary morbidity was identified in 18/64 (28%) of those with abnormal LFTs. 6 patients (1.6%) had PSC, of whom 5 had raised ALP. <h3>Conclusion</h3> More than one in six patients with IBD in this cohort had abnormal hepatic biochemistry and of these, over a quarter had identifiable hepatobiliary morbidity. Surprisingly, the prevalence of abnormal LFTs was higher than expected in African-Caribbean patients and low in South Asians. IBD type and phenotype was not associated with abnormal liver biochemistry. Confirmation and further evaluation of these findings should be sought prospectively in an independent cohort.
Increase in antibiotic resistance in Haemophilus influenzae in the United Kingdom since 1977: report of study group.
Authors: J Philpott-Howard, J D Williams
Journal: BMJ (1982)

A survey of antibiotic resistance in Haemophilus influenzae was carried out in the United Kingdom with 25 laboratories participating. The incidence of resistance in the 1841 strains examined was: tetracycline 3.1%, ampicillin 6.2%, chloramphenicol 1.03%, trimethoprim 1.4%, and sulphamethoxazole 1.5%. Of the 115 strains resistant to ampicillin, 106 produced beta-lactamase. Seventy-nine strains were capsulate, none of which was chloramphenicol resistant, but nine produced beta-lactamase (11.4%). Comparison of these figures of antibiotic resistance with those from a similar survey performed in 1977 showed a significant increase in resistance of H influenzae to ampicillin, chloramphenicol, and trimethoprim.
Consent to the publication of patient information: Seeking consent is morally essential
Authors: Fiona M Woollard
Journal: BMJ (2004)

EDITOR—Singer writes: “For this reason, you must obtain express consent from patients before publishing personal information about them as individuals in media to which the public has access, for example in journals or text books, whether or not you believe the patient can be identified. Express consent must therefore be sought to the publication of, for example, case-histories about, or photographs of, patients.

“However, the GMC does admit of exceptions in the case of patients who have …
Can Physician Profiles Be Trusted?
Authors: Andrew B. Bindman
Journal: JAMA (1999)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2022 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
Clinical Outcome of Nonculprit Plaque Ruptures in Patients With Acute Coronary Syndrome in the PROSPECT Study
Authors: Yong Xie, Gary S. Mintz, Junqing Yang, Hiroshi Doi, Andrés Iñiguez, George D. Dangas, Patrick W. Serruys, John A. McPherson, Bertil Wennerblom, Ke Xu, Giora Weisz, Gregg W. Stone, Akiko Maehara
Journal: JACC. Cardiovascular imaging (2014)
Radiation exposure and the protection of the community.
Authors: D Gloag
Journal: BMJ (1980)

Decisions about nuclear power clearly entail value judgments. But the issues also have to be looked at in the wider context of radiation exposure from all sources?and in the context too of controversy about the theoretical aspects. Radiation dose limits are recommended by the International Commission on Radio logical Protection,1 but some people are arguing that they are set too high.2 Epidemiological evidence, as discussed in the last article (p 1479), does not show clearly how we should extrapolate from the long-term effects of high or moderate radiation doses to those of low doses.3 Authorities differ in the weight they attach to experimental data, but neither do these at present permit a definite decision between the different possible dose-response models (effect proportionate to the dose or to the square of the dose, for example) : we first need fuller knowledge of the pro cesses of cancer development in man.4 According to the most widely held view, however, the cellular and other mechanisms indicated by radiobiological research strongly suggest that the risk from low doses of low-LET (linear-energy-transfer) radi ation is not underestimated by linear extrapolation from the risk at moderate levels?it may be somewhat (perhaps considerably) overestimated.5 For low doses of high-LET radiation on the other hand a linear extrapolation is likely to give good estimates. High doses of any radiation kill many cells?in fact they may preferentially kill transformed cells6?and so cancers are likely to be relatively fewer, with a turn-down of the dose-response curve (fig 1, last article, p 1480). According to most (but not all) of the data on animals ex posed to low-LET radiation, linear extrapolation does give an overestimation of risk for low doses or dose rates.7 This is explained on the grounds that cellular repair mechanisms can make good much of the damage to the DNA produced by low level low-LET radiation. Radford,4 who?though chairman of the carcinogenic effects subcommittee?presents a dissenting view in the third report of the Biological Effects of Ionising Radiations Committee (BEIR III), comments that the com mittee was strongly influenced by animal studies in adopting the intermediate linear-quadratic dose-response model. He points out the well-known limitations of work on animals: for example, they may have different types of tumours, with perhaps quantitatively different mechanisms in response to radiation; they have a shorter life span than man in which to develop tumours; and in a laboratory environment they are little exposed to cancer-promoting agents, so that radiation must be sufricient to act as a complete carcinogen and not just an initiator. Unlike genetic defects, where the BEIR Committee does consider that risk is proportionate to dose, many processes (probably differing in importance from species to species) are accepted as modifying or facilitating the development of tumours once the initial damage has occurred; they include immuno
Anoikis-resistant MDA-MB-231 cells: characteristics and pathway analysis.
Authors: J Yu, W Han, J Kim, J Lee, E Ko, E Kim, H Moon, D Noh
Journal: Cancer Research (2009)

Abstract Abstract #2062 Background : Apoptosis in response to inappropriate adhesion or lack of adhesion has been termed anoikis. Resistance to anoikis is regarded as a prerequisite for invasion and metastasis in cancer cells. Recently many studies were performed to understand mechanism of anoikis resistance. However, there have been few studies on the role and mechanism of anoikis resistance in cancer cells.&amp;#x2028; Materials and Methods : Anoikis-resistant MDA-MB-231 cells were induced and selected through culture on polyhydroxyethylmethacrylate (Poly-HEMA) substratum and invasiveness by matrigel invasion assay and drug-resistance to doxorubicin were checked. At the same time, expression of genes were evaluated in anoikis-resistant and adherent MDA-MB-231 cells by cDNA microarray. Pathway analysis on high-expressed genes in anoikis-resistant cells was performed by software(Ingenuity Pathway Analysis)&amp;#x2028; Results : Invasion assays revealed that anoikis-resistant cells were more invasive than adherent cells. Anoikis-resistant cells were also more resistant to doxorubicin than adherent cells. Genes related to NF-kB pathway were highly expressed in anoikis-resistant cells. Therefore, the effect of Bay11-7085, inhibitor of NF-kB, on the growth of anoikis-resistant MDA-MB-231 cells was tested. The blockage of NF-kB pathway inhibited the growth of anoikis-resistant MDA-MB-231 cells.&amp;#x2028; Conclusion : These results demonstrated that anoikis resistance was associated with increased invasiveness and resistance to chemotherapeutic agents and that NF-kB pathway involved in anoikis resistance. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 2062.
Recognising hiatus hernia.
Authors: J R Graham
Journal: BMJ (1976)

Myasthenic syndrome during treatment with practolol SIR,-The myasthenic syndrome during treat- ment with large doses of practolol described by Drs R 0 Hughes and F J Zacharias (21 February, p 460) appears to be a clinical manifestation of the effect of 3-adrenoceptor blocking agents on the neuromuscular junction observed in animals.Like other members of this group of drugs' 2 practolol has a curare- like action, as shown in sciatic nerve- gastrocnemius preparations of the cat:' and frog and in the frog sciatic nerve-sartorius preparation and rectus abdominis muscle.2 4 The dosage required to depress neuromuscular transmission was larger for practolol than for propranolol.Though the patient's electromyogram, presumably taken in the resting state, was normai, it would be of great interest to know whether in the myasthenic state repetitive nerve stimulation evoked a gradually declining response of the muscle and whether even in the absence of the myasthenic syndrome the patient was particularly prone to fatigue.As in experimental animals the neuromuscular effects of '3-adrenoceptor blockers are readily reversible the risk of a relapse of the myas- thenic syndrome seems to be remote.How- ever, the patient may be hypersensitive to D-tubocurarine and related agents and also to drugs with a local anaesthetic action, like quinidine.