tbuckley/cabot-search huggingface dataset:
Pacemaker induced ventricular fibrillation in coronary care units
Authors: Andrew A McLeod, Percy P Jokhi
Journal: BMJ (2004)

Temporary transvenous pacing is an established treatment for many bradyarrhythmias associated with haemodynamic compromise in patients who have had acute myocardial infarction. Procedural complications associated with insertion of temporary pacing electrodes are well recognised and documented, as is subsequent loss of capture due to rising stimulation threshold or electrode displacement.1 Temporary transvenous pacing, if not applied correctly, may also directly provoke ventricular arrhythmias. Here we report two cases of ventricular fibrillation that were caused by a temporary pacemaker in a coronary care unit.

### Case 1

A 64 year old man was admitted to the coronary care unit with acute inferior myocardial infarction. He was noted to be hypotensive and have a nodal rhythm with no atrial activity at 30 beats/min. There was no response to atropine. A temporary pacing electrode was inserted and connected to an external ventricular demand pacemaker. During the following two days, at least 15 episodes of ventricular fibrillation and many sustained episodes of ventricular tachycardia occurred. Review of the electrocardiograms showed occasional failure of pacing and sensing and of pacing impulses delivered into the ST segment and the T wave of spontaneous beats causing ventricular fibrillation (fig 1). The pacemaker was turned off. A bradycardia with first degree atrioventricular block was noted, but the episodes of ventricular fibrillation stopped immediately and did not recur.



Fig 1 
Case 1. Top: Apparently satisfactory pacing (first QRS complex) is followed by fusion beats, but failure to sense becomes apparent when the pacemaker spike (narrow artefact) discharges into the ST segment. The first captured premature complex leads to ventricular tachycardia, which later degenerates into ventricular fibrillation. Further pacing spikes …
Inhibition of human leukemia in an animal model with human antibodies directed against vascular endothelial growth factor receptor 2. Correlation between antibody affinity and biological activity
Authors: Z Zhu, K Hattori, H Zhang, X Jimenez, D L Ludwig, S Dias, P Kussie, H Koo, H J Kim, D Lu, M Liu, R Tejada, M Friedrich, P Bohlen, L Witte, S Rafii
Journal: Leukemia (2003)
93 ATGL (PNPLA2) KNOCKOUT MICE ARE PROTECTED FROM HEPATIC ER-STRESS VIA OLEIC ACID ACCUMULATION
Authors: C.D. Fuchs, T. Claudel, P. Kumari, T. Stojakovic, G. Haemmerle, E. Halilbasic, J. Gumhold, D. Silbert, H. Koefeler, R. Zechner, M. Trauner
Journal: Journal of Hepatology (2011)
Miltefosine — The Long-Awaited Therapy for Visceral Leishmaniasis?
Authors: Barbara L. Herwaldt
Journal: New England Journal of Medicine (1999)

Miltefosine was originally developed as an antineoplastic drug, but it has the potential to become the first highly effective, orally administered drug for treating visceral leishmaniasis, a life-threatening parasitic disease. We do not know whether additional clinical trials and experience with miltefosine will support the encouraging findings of the phase 2 study described by Jha et al. in this issue of the Journal. 1 However, the prospect of a new drug that is administered orally rather than parenterally is good news indeed, because the drug could markedly facilitate the treatment of patients.Although asymptomatic or subclinical infection is common in some . . .
The Hemodynamic Effects of Treatment with Interleukin-2 and Lymphokine-Activated Killer Cells
Authors: Ellen R. Gaynor
Journal: Annals of Internal Medicine (1988)

Study Objective: To determine the hemodynamic alterations occurring during therapy with the maximally tolerated doses of interleukin-2 and lymphokine-activated killer cells. Design: Case series. Setting: Referral-based inpatient oncology service at a university medical center. Patients: A sequential sample of 13 patients with metastatic colon carcinoma, malignant melanoma, or hypernephroma who were receiving treatment with interleukin-2 and lymphokine-activated killer cells in the maximally tolerated doses. Measurements and Main Results: Pretreatment variables of mean arterial pressure, systemic vascular resistance, heart rate, pulmonary capillary wedge pressure, and cardiac index were compared with the same variables measured either immediately before the eighth dose of interleukin-2 or immediately before the initiation of pressor support with dopamine hydrochloride. When these values were compared with the pretreatment values, patients showed a significant decrease in mean arterial pressure (92 mm Hg compared with 75 mm Hg; P < 0.0001), and systemic vascular resistance (15.1 compared with 8.5 mm Hg/L · min; P < 0.0001), but an increase in heart rate (73 compared with 110 beats/min; P < 0.0001) and cardiac index (3.1 compared with 4.7 L/min · m2 body surface area; P < 0.0001). No significant change was noted in pulmonary capillary wedge pressure. Low systemic vascular resistance persisted throughout interleukin-2 therapy. Although blood pressure normalized in 24 hours, the systemic vascular resistance remained below baseline levels 6 days after interleukin therapy had been stopped. Interventions: Blood pressure was successfully supported at greater than 90 mm Hg with dopamine hydrochloride or phenylephrine hydrochloride, or both. Conclusions: Therapy with high doses of interleukin-2 induces hemodynamic changes consistent with a high-output and low-resistance state similar to changes noted during the early phase of septic shock.
Angioimmunoblastic lymphadenopathy associated with polyarthritis.
Authors: R S Rothwell, M J Mant, P Davis
Journal: Annals of the Rheumatic Diseases (1980)

A patient with angioimmunoblastic lymphadenopathy with dysproteinaemia is described. The patient had a severe clinical illness with a pronounced haemolytic anaemia, which followed well-established polyarthritis and gold therapy. It was accompanied by in-vitro evidence of suppressed cell-mediated immune responses and by development of serum antismooth muscle antibodies. These features are unusual and support theories that this disease has an immunological basis. Improvement occurred with prednisone and azathioprine therapy, suggesting that combined use of these agents is useful in some patients with AILD. The patient subsequently developed a lymphoma.
Dependence of hypoxic cellular calcium loading on Na(+)-Ca2+ exchange.
Authors: M C Haigney, H Miyata, E G Lakatta, M D Stern, H S Silverman
Journal: Circulation Research (1992)

Na(+)-Ca2+ exchange has been shown to contribute to reperfusion- and reoxygenation-induced cellular Ca2+ loading and damage in the heart. Despite the fact that both [Na+]i and [Ca2+]i have been documented to rise during ischemia and hypoxia, it remains unclear whether the rise in [Ca2+]i occurring during hypoxia is linked to the rise in [Na+]i via Na(+)-Ca2+ exchange before reoxygenation and how this relates to cellular injury. Single electrically stimulated (0.2 Hz) adult rat cardiac myocytes loaded with Na(+)-sensitive benzofuran isophthalate (SBFI), the new fluorescent probe, were exposed to glucose-free hypoxia (PO2 less than 0.02 mm Hg), and SBFI fluorescence was monitored to index changes in [Na+]i. Parallel experiments were performed with indo-1-loaded cells to index [Ca2+]i. The SBFI fluorescence ratio (excitation, 350/380 nm) rose significantly during hypoxia after the onset of ATP-depletion contracture, consistent with a rise in [Na+]i. At reoxygenation, the ratio fell rapidly toward baseline levels. The indo-1 fluorescence ratio (emission, 410/490 nm) also rose only after the onset of rigor contracture and then often showed a secondary rise early after reoxygenation at a time when [Na+]i fell. The increase in both [Na+]i and [Ca2+]i, seen during hypoxia, could be markedly reduced by performing experiments in Na(+)-free buffer. These experiments suggested that hypoxic Ca2+ loading is linked to a rise in Na+i via Na(+)-Ca2+ exchange. To show that Na(+)-Ca2+ exchange activity was not fully inhibited by profound intracellular ATP depletion, cells were exposed to cyanide, and then buffer Na+ was abruptly removed after contracture occurred. The sudden removal of buffer Na+ would be expected to stimulate cell Ca2+ entry via Na(+)-Ca2+ exchange. A large rapid rise in the indo-1 fluorescence ratio ensued, which was consistent with abrupt cell Ca2+ loading via the exchanger. The effect of reducing hypoxic buffer [Na+] on cell morphology after reoxygenation was examined. Ninety-five percent of cells studied in a normal Na(+)-containing buffer (144 mM NaCl, n = 38) and reoxygenated 30 minutes after the onset of hypoxic rigor underwent hypercontracture. Only 12% of cells studied in Na(+)-free buffer (144 mM choline chloride, n = 17) hypercontracted at reoxygenation (p less than 0.05). Myocytes were also exposed to hypoxia in the presence of R 56865, a compound that blocks noninactivating components of the Na+ current. R 56865 blunted the rise in [Na+]i typically seen after the onset of rigor, suggesting that Na+ entry may occur, in part, through voltage-gated Na+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)
First-Trimester Drug Use and Congenital Disorders
Authors: Hershel Jick, Lewis B. Holmes, Judith R. Hunter, Sue Madsen, Andy Stergachis
Journal: JAMA (1981)

We determined the prevalence of certain major congenital disorders among the infants of women who used a wide variety of drugs during the first trimester of pregnancy in a prepaid health plan in which automated recording of prescriptions filled and disorders diagnosed at birth was available. No strong associations between any of the commonly used drugs and congenital disorders studied were present. (<i>JAMA</i>1981;246:343-346)
984-29 Modulation of s-Homocysteine Associated with Intimal Thickening After Balloon Angioplasty Injury of the Rabbit Iliac Artery
Authors: Karel K.J. Kuiper, Keith A. Robinson, Elisabeth Schieffer, Nicolas A.F. Chronos, Helga Refsum, Jan-Erik Nordrehaug
Journal: Journal of the American College of Cardiology (1995)
Ventricular Fibrillation during Interim Pacing of the Heart by a Bipolar Endocardial Electrode
Authors: S. Moulopoulos, K. Kehayoglou, S. Stamatelopoulos, D. Sideris
Journal: New England Journal of Medicine (1964)

ELECTROCUTION during the application of cardiac pacemakers has been reported by several authors.1 2 3 4 5 Interference between pacemaker stimuli and heart impulses has not been considered a common source of complications. Elmqvist et al.4 reported ventricular fibrillation in 2 patients with an implanted pacemaker or an external one directly applied to the heart after a thoracotomy. The effect of currents originating from improperly grounded external appliances, connected to the patient, has also been pointed out.6 The use of a soldering iron5 was considered to be responsible for the appearance of ventricular fibrillation in 1 patient, whose heart was driven by an external . . .
Government to review doctors' revalidation system
Authors: Zosia Kmietowicz
Journal: BMJ (2004)

The General Medical Council has postponed the introduction of its new system for assessing doctors' fitness to practise after the government asked to review the scheme because of criticisms of it (on p 10) in the fifth report of the Shipman inquiry.

The council's new scheme of revalidation will be shelved until the review is complete, which will not be until after the scheme was due to be …
Sister Mary Joseph Nodule in Endometrial Carcinoma
Authors: Harmandeep Singh, Punit Sharma, Rama Mohan Reddy, Chandrasekhar Bal, Arun Malhotra, Rakesh Kumar
Journal: Clinical Nuclear Medicine (2013)

Sister Mary Joseph nodules are very rare. They are commonly caused by gastrointestinal tract and ovarian cancers, but they are seen rarely in uterine carcinoma, lung carcinoma, breast carcinoma, and others. We present F-FDG PET/CT findings in a 55-year-old woman with endometrial adenocarcinoma, who presented with a mass protruding from the umbilicus after surgery and pelvic radiotherapy.
The head-regeneration transcriptome of the planarian Schmidtea mediterranea
Authors: Thomas Sandmann, Matthias C Vogg, Suthira Owlarn, Michael Boutros, Kerstin Bartscherer
Journal: Genome biology (2011)

Abstract Background Planarian flatworms can regenerate their head, including a functional brain, within less than a week. Despite the enormous potential of these animals for medical research and regenerative medicine, the mechanisms of regeneration and the molecules involved remain largely unknown. Results To identify genes that are differentially expressed during early stages of planarian head regeneration, we generated a de novo transcriptome assembly from more than 300 million paired-end reads from planarian fragments regenerating the head at 16 different time points. The assembly yielded 26,018 putative transcripts, including very long transcripts spanning multiple genomic supercontigs, and thousands of isoforms. Using short-read data from two platforms, we analyzed dynamic gene regulation during the first three days of head regeneration. We identified at least five different temporal synexpression classes, including genes specifically induced within a few hours after injury. Furthermore, we characterized the role of a conserved Runx transcription factor, smed-runt-like1 . RNA interference (RNAi) knockdown and immunofluorescence analysis of the regenerating visual system indicated that smed-runt-like1 encodes a transcriptional regulator of eye morphology and photoreceptor patterning. Conclusions Transcriptome sequencing of short reads allowed for the simultaneous de novo assembly and differential expression analysis of transcripts, demonstrating highly dynamic regulation during head regeneration in planarians.
Discord among proponents of rival allergy desensitization techniques
Authors: W. Check
Journal: JAMA (1980)

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 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
Trainees' Retention of Cardiopulmonary Resuscitation
Authors: Frank J. Weaver
Journal: JAMA (1979)

Lay persons trained in cardiopulmonary resuscitation (CPR) were evaluated six months after completion of a four-hour basic life support course to determine the degree to which CPR cognitive and psychomotor performance skills were retained. Evaluation criteria were based on the American Heart Association's recommended standards. The data disclosed a significant decrease in the resuscitators' retention of CPR knowledge and skills.
Abstract A41: Harnessing neural stem cell tumor tropism for targeted nanoparticle delivery: Potential for ovarian cancer therapy
Authors: Rachael Mooney, Megan Gilchrist, Yiming Weng, Alexander Annala, Sukhada Bhojane, Elizabeth Garcia, Luella Roma, Kenna Schnarr, Thanh Dellinger, Ernest Han, Aboody S. Karen, Jacob M. Berlin
Journal: Clinical Cancer Research (2013)

Abstract Intraperitoneal as compared to intravenous administration of chemotherapy has shown improved survival rates for stage III ovarian cancer. While this demonstrates that concentrating chemotherapy at the tumors has therapeutic benefit, intraperitoneal therapy was also accompanied by significantly increased toxic side effects. There is thus an urgent need for a targeted delivery system that could localize therapy at the tumors and decrease the side-effects. Here we show that stem cell/nanoparticle hybrids may be used for such targeted therapy. In pre-clinical brain and other invasive and metastatic tumor models, neural stem cells have been shown to overcome a variety of biological barriers and migrate selectively to invasive tumor foci, even penetrating hypoxic tumor regions. Here we present data confirming that neural stem cells also migrate selectively to ovarian cancer. Moreover, the neural stem cells can engineered to transport to the tumors nanoparticles that either contain chemotherapy drugs or can be induced to heat. The combination of neural stem cells and nanoparticles that can either be used for thermal ablation or slowly release chemotherapy drugs offers the potential to realize a modular and general drug targeting system for the treatment of stage III ovarian cancer. Citation Format: Rachael Mooney, Megan Gilchrist, Yiming Weng, Alexander Annala, Sukhada Bhojane, Elizabeth Garcia, Luella Roma, Kenna Schnarr, Thanh Dellinger, Ernest Han, Aboody S. Karen, Jacob M. Berlin. Harnessing neural stem cell tumor tropism for targeted nanoparticle delivery: Potential for ovarian cancer therapy. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: From Concept to Clinic; Sep 18-21, 2013; Miami, FL. Philadelphia (PA): AACR; Clin Cancer Res 2013;19(19 Suppl):Abstract nr A41.
Hyperkalemia and Trimethoprim-Sulfamethoxazole
Authors: Mark G. Parker
Journal: Annals of Internal Medicine (1996)

Letters1 November 1996Hyperkalemia and Trimethoprim-SulfamethoxazoleMark G. Parker, MDMark G. Parker, MDLahey Hitchcock Clinic Burlington, MA 01805.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-9-199611010-00022 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:The recent study by Alappan and colleagues [1] draws appropriate attention to the potential and perhaps little-known problem of hyperkalemia during treatment with trimethoprim-sulfamethoxazole in hospitalized patients. The authors attribute the observed impairment in potassium excretion primarily to the amiloride-like actions of trimethoprim in the distal tubule, and they note concurrent renal insufficiency as an associated risk factor. They fail to comment, however, on an important element of the pathogenesis of this disorder, that is, the influence of nutritional intake, obligate daily osmolar excretion, and urine volume on potassium excretion.Acutely ill patients generally do not have ...References1. Alappan R, Perazella MA, Buller GK. Hyperkalemia in hospitalized patients treated with trimethoprim-sulfamethoxazole. Ann Intern Med. 1996; 124:316-20. Google Scholar2. Keusch GT, Farthing MJG. Nutrition and infection. Ann Rev Nutr. 1986; 6:131-54. Google Scholar3. Ethier JH, Kamel KS, Magner PO, Lemann JJ, Halperin ML. The transtubular potassium concentration in patients with hypokalemia and hyperkalemia. Am J Kidney Dis. 1990; 15:309-15. Google Scholar Author, Article, and Disclosure InformationAuthors: Mark G. Parker, MDAffiliations: Lahey Hitchcock Clinic Burlington, MA 01805. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byIs it time for oncologists to modify their laissez-faire attitude toward alternative/ complementary ‘drug therapy’? 1 November 1996Volume 125, Issue 9Page: 778-779KeywordsExcretionNutritionNutritional deficienciesOutpatientsPathogenesisPotassiumProteinsSodium chlorideUreaUrine ePublished: 15 August 2000 Issue Published: 1 November 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
False-Positive WBC Imaging Secondary to a Distended Bladder and Fecal Retention
Authors: GARY E. MEYERROSE, CRAIG CARTER, GLENN H. ROBERSON
Journal: Clinical Nuclear Medicine (1997)

In an attempt to identify a focus of infection, WBC scintigraphy was performed, and it showed increased accumulation in the midanterior pelvis suspicious for a site of infection. Computed tomography of the pelvis obtained after WBC scintigraphy showed gross retention of stool and a distended bladder, but no suggestion of infection. Repeat WBC scintigraphy performed with a Foley catheter in place after bowel cleansing did not show any abnormal tracer accumulation. This case shows how the combination of a distended bladder and fecal retention can produce images suggestive of a site of infection.
Iron uptake by human upper small intestine microvillous membrane vesicles. Indication for a facilitated transport mechanism mediated by a membrane iron-binding protein.
Authors: R Teichmann, W Stremmel
Journal: Journal of Clinical Investigation (1990)

To investigate the hypothesis that iron absorption in man involves a carrier-mediated cellular uptake mechanism, influx velocity (Vo) of 59Fe3+ by isolated human microvillous membrane (MVM) vesicles of the upper small intestine was examined. Vo revealed saturation kinetics (Km = 315 nM; Vmax = 361 pmol Fe3+ x min-1 x mg protein-1) was temperature dependent and inhibited by pronase pretreatment of MVM. In the presence of an inwardly directed Na(+)-gradient a typical overshoot phenomenon with maximal uptake at 30-40 s was observed. The suggestion of an active, carrier-mediated uptake mechanism for iron was pursued by isolation of a 160-kD iron-binding protein from solubilized human MVM proteins. This glycoprotein was assembled as a trimer composed of 54-kD monomers. A monospecific antibody against the 54-kD subunit inhibited vesicular influx of Fe3+ into MVM by greater than 50%. Immunofluorescence and immunoblot analysis confirmed the localization of the protein in brush border plasma membranes. It was detectable in human intestinal mucosa and liver, but not in esophagus. These data indicate that the translocation of Fe3+ across human MVM represents a facilitated transport mechanism which is, at least in part, mediated by a membrane iron-binding protein.