tbuckley/cabot-search huggingface dataset:
House-Staff Training — The Need for Careful Reform
Authors: R M Glickman
Journal: New England Journal of Medicine (1988)

As the director of an internal medicine training program in a large urban academic medical center, I have mixed feelings about the regulations proposed by the New York State Health Department to modify the hours and supervision of house staffs.I often find myself trying to balance the educational content of residency training with the escalating demands of patient care. I am acutely aware of the effects of burgeoning service requirements - at the expense of time devoted to education - on house-staff morale. I compare my own house-staff training in the mid-1960s with the program I now administer, and . . .
Gallium-67 Studies in a Patient with Multiple Muscular Abscesses
Authors: JEAN F. BOUVIER, BERNARD BOCQUET, BADRE E. LAHNECHE
Journal: Clinical Nuclear Medicine (1986)

A 45-year-old diabetic was admitted with one-week history of fever and muscular pains. He had not had any trauma. On physical examination he had a firm mass within the anterior left thigh. A puncture yielded Staphylococcus aureus. Urine cultures showed the same organism, but blood cultures were negative. The patient was treated with parenteral cefalotine and netilmicin. Lymphatic and venous inflammations appeared in the left forearm after one injection. Whole-body tomoscans and spot scintiphotos were obtained at 48 hours following the administration of 185 MBq of Ga-67 citrate intravenously. The images revealed focal concentrations of radiotracer in both right and left thighs and the right elbow. They were all muscular abscesses. The diagnosis was confirmed by CT. An increased uptake of radiotracer also was localized along the inflammatory radial vein in the left forearm. In the evaluation of muscular pains with fever, Ga-67 studies may be of value in detecting scattered muscular abscesses.
Hemodynamic factors that affect calculated orifice areas in the mitral hancock xenograft valve.
Authors: J L Ubago, A Figueroa, T Colman, A Ochoteco, C G Duran
Journal: Circulation (1980)

From June 1974 to December 1978, 714 Hancock valves have been placed in 605 patients. One hundred seventy-five patients with a mitral xenograft have been restudied. The results were questionable due to the wide scatter and disparity between the calculated and the theoretical orifice of each valve size. To elucidate these differences, the hemodynamic data of 40 isolated, normal functioning mitral Hancock valves were reviewed. Early, middle and late diastolic mitral valve gradients were measured by planimetry and their corresponding flows were estimated by angiography. The paired data were fitted to exponential functions and specific lines for each Hancock valve size were obtained. By superimposing Gorlin's pressure and flow curves on these lines, the instantaneous effective orifice for each Hancock valve can be determined. We concluded that 1) the Hancock valve effective orifice is flow related and always lower than its theoretical opening; 2) normal function frequently cannot be firmly established by the mean effective area; and 3) the nomogram described may help in determining the time-related variations of a particular valve.
Cytotoxic T cells transduced with chimeric anti-CD19 receptors prevent engraftment of primary lymphoblastic leukemia in vivo
Authors: S Landmeier, B Altvater, S Pscherer, J Meltzer, N Sebire, M Pule, J Vera, M Hotfilder, H Juergens, J Vormoor, C Rossig
Journal: Leukemia (2010)
In Support of SUPPORT — A View from the NIH
Authors: Kathy L. Hudson, Alan E. Guttmacher, Francis S. Collins
Journal: New England Journal of Medicine (2013)

In the wake of extensive scientific and public discussions since our March 7, 2013, determination letter in the SUPPORT study, OHRP has become aware of widespread misunderstanding about the risks that are required to be disclosed in obtaining informed consent for certain types of clinical trials.Our goal in this letter is to clarify several issues related to our determination.At the outset, we wish to emphasize that OHRP does not and has never questioned whether the design of the SUPPORT study was ethical.It was a study that asked important questions and produced information that promises to advance both scientific knowledge and clinical care.Rather, consistent with OHRP's mission to protect human subjects of research, the overarching concern of our determination was the adequacy of informed consent, a bedrock principle of research involving human subjects.To make truly informed decisions about whether or not to participate in a research study, potential volunteers or their parents or guardians are entitled to certain information, including a description of reasonably foreseeable risks.We acknowledge that the UAB consent form included language that reflected then-current research suggesting that lower saturation targets reduced the risk of retinopathy of prematurity (ROP), as well as language about the potential risks of ROP with prolonged use of supplemental oxygen.However, the "Risks" section of that form failed to mention and appropriately describe, as it should have, that relationship.More
SYPHILIS IN THE NEGRO.
Authors: FRANK JONES
Journal: JAMA (1904)

With the advent of his emancipation and his citizenship the negro earned his syphilis and bequeathed it (both by acquisition and heredity) to his posterity, to such a degree that he, in a great measure, became syphilized prior to his becoming civilized. Syphilis obtains in all of its forms in its most classic type in the negro by reason of his habits, his environments, his utter indifference to the disease and his carelessness and delay in having it treated. My experience, covering a period of more than six years in a large clinic composed almost entirely of negroes, justifies me in making the statement that 75 per cent. of that class of negroes who come as patients are syphilitic (either acquired or hereditary) . I could present you with a museum of Jonathan Hutchinson's teeth, bridge-shaped noses, rickets, and Parott's disease, showing the result of herditary syphilis in negro children.
Spontaneous Remission of Retinitis in a Case of Infection with Human Immunodeficiency Virus Type 1 (HIV-1)
Authors: Ronald G. Nahass
Journal: Annals of Internal Medicine (1988)

Letters and Corrections15 July 1988Spontaneous Remission of Retinitis in a Case of Infection with Human Immunodeficiency Virus Type 1 (HIV-1)Ronald G. Nahass, MD, David Alcid, MD, David J. Gocke, MDRonald G. Nahass, MDSearch for more papers by this author, David Alcid, MDSearch for more papers by this author, David J. Gocke, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-109-2-168_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor: We agree with Dr. Whitley (1) that, despite the lack of controlled trials on the use of ganciclovir in cytomegalovirus chorioretinitis, data suggest it is beneficial. We report a case that shows the need for placebo-controlled trials for cytomegalovirus-related disease.A 30-year-old male intravenous drug user with group 4 human immunodeficiency virus type 1 (HIV-1) infection had multiple scotomata that had developed over a 2-week period. Funduscopic examination showed bilateral perivascular retinal hemorrhages and pale yellow plaques. Serum IgG titer for cytomegalovirus was positive at 1:32 dilution. A urine culture for cytomegalovirus was also positive. Azidothymidine treatment...References1. Whitley R. Ganciclovir—have we established clinical value in the treatment of cytomegalovirus infection? Ann Intern Med 1988;108:452-4. LinkGoogle Scholar2. Laskin O, Cederberg D, Mills J, Eron L, Milduan D, and Spector S. Ganciclovir for the treatment and suppression of serious infections caused by cytomegalovirus. Am J Med. 1987;83:201-7. CrossrefMedlineGoogle Scholar3. Pomerantz R, Kuritzkes D, and De La Monte S. Infection of the retina by human immunodeficiency virus type 1. N Engl J Med. 1987;317:1643-7. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Ronald G. Nahass, MD; David Alcid, MD; David J. Gocke, MDAffiliations: University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School New Brunswick, NJ 08901 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 July 1988Volume 109, Issue 2Page: 168-168KeywordsAddictsAzidothymidineCytomegalovirus infectionHemorrhageHIV-1RetinitisUrine ePublished: 1 December 2008 Issue Published: 15 July 1988 PDF downloadLoading ...
CMR-Based Differentiation of AL and ATTR Cardiac Amyloidosis
Authors: Jason N. Dungu, Oswaldo Valencia, Jennifer H. Pinney, Simon D.J. Gibbs, Dorota Rowczenio, Janet A. Gilbertson, Helen J. Lachmann, Ashutosh Wechalekar, Julian D. Gillmore, Carol J. Whelan, Philip N. Hawkins, Lisa J. Anderson
Journal: JACC. Cardiovascular imaging (2014)
Role of Ca <sup>2+</sup> /Calmodulin-Stimulated Cyclic Nucleotide Phosphodiesterase 1 in Mediating Cardiomyocyte Hypertrophy
Authors: Clint L. Miller, Masayoshi Oikawa, Yujun Cai, Andrew P. Wojtovich, David J. Nagel, Xiangbin Xu, Haodong Xu, Vince Florio, Sergei D. Rybalkin, Joseph A. Beavo, Yiu-Fai Chen, Jian-Dong Li, Burns C. Blaxall, Jun-ichi Abe, Chen Yan
Journal: Circulation Research (2009)

Cyclic nucleotide phosphodiesterases (PDEs) through the degradation of cGMP play critical roles in maintaining cardiomyocyte homeostasis. Ca(2+)/calmodulin (CaM)-activated cGMP-hydrolyzing PDE1 family may play a pivotal role in balancing intracellular Ca(2+)/CaM and cGMP signaling; however, its function in cardiomyocytes is unknown.Herein, we investigate the role of Ca(2+)/CaM-stimulated PDE1 in regulating pathological cardiomyocyte hypertrophy in neonatal and adult rat ventricular myocytes and in the heart in vivo.Inhibition of PDE1 activity using a PDE1-selective inhibitor, IC86340, or downregulation of PDE1A using siRNA prevented phenylephrine induced pathological myocyte hypertrophy and hypertrophic marker expression in neonatal and adult rat ventricular myocytes. Importantly, administration of the PDE1 inhibitor IC86340 attenuated cardiac hypertrophy induced by chronic isoproterenol infusion in vivo. Both PDE1A and PDE1C mRNA and protein were detected in human hearts; however, PDE1A expression was conserved in rodent hearts. Moreover, PDE1A expression was significantly upregulated in vivo in the heart and myocytes from various pathological hypertrophy animal models and in vitro in isolated neonatal and adult rat ventricular myocytes treated with neurohumoral stimuli such as angiotensin II (Ang II) and isoproterenol. Furthermore, PDE1A plays a critical role in phenylephrine-induced reduction of intracellular cGMP- and cGMP-dependent protein kinase (PKG) activity and thereby cardiomyocyte hypertrophy in vitro.These results elucidate a novel role for Ca(2+)/CaM-stimulated PDE1, particularly PDE1A, in regulating pathological cardiomyocyte hypertrophy via a cGMP/PKG-dependent mechanism, thereby demonstrating Ca(2+) and cGMP signaling cross-talk during cardiac hypertrophy.
Comorbidity and repeat admission to hospital for adverse drug reactions in older adults: retrospective cohort study
Authors: M. Zhang, C D. J Holman, S. D Price, F. M Sanfilippo, D. B Preen, M. K Bulsara
Journal: BMJ (2009)

<b>Objectives</b> To identify factors that predict repeat admission to hospital for adverse drug reactions (ADRs) in older adults. <b>Design</b> Population based retrospective cohort study. <b>Setting</b> All public and private hospitals in Western Australia. <b>Participants</b> 28 548 patients aged ≥60 years with an admission for an ADR during 1980-2000 followed for three years using the Western Australian data linkage system. <b>Results</b> 5056 (17.7%) patients had a repeat admission for an ADR. Repeat ADRs were associated with sex (hazard ratio 1.08, 95% confidence interval 1.02 to 1.15, for men), first admission in 1995-9 (2.34, 2.00 to 2.73), length of hospital stay (1.11, 1.05 to 1.18, for stays ≥14 days), and Charlson comorbidity index (1.71, 1.46 to 1.99, for score ≥7); 60% of comorbidities were recorded and taken into account in analysis. In contrast, advancing age had no effect on repeat ADRs. Comorbid congestive cardiac failure (1.56, 1.43 to 1.71), peripheral vascular disease (1.27, 1.09 to 1.48), chronic pulmonary disease (1.61, 1.45 to 1.79), rheumatological disease (1.65, 1.41 to 1.92), mild liver disease (1.48, 1.05 to 2.07), moderate to severe liver disease (1.85, 1.18 to 2.92), moderate diabetes (1.18, 1.07 to 1.30), diabetes with chronic complications (1.91, 1.65 to 2.22), renal disease (1.93, 1.71 to 2.17), any malignancy including lymphoma and leukaemia (1.87, 1.68 to 2.09), and metastatic solid tumours (2.25, 1.92 to 2.64) were strong predictive factors. Comorbidities requiring continuing care predicted a reduced likelihood of repeat hospital admissions for ADRs (cerebrovascular disease 0.85, 0.73 to 0.98; dementia 0.62, 0.49 to 0.78; paraplegia 0.73, 0.59 to 0.89). <b>Conclusions</b> Comorbidity, but not advancing age, predicts repeat admission for ADRs in older adults, especially those with comorbidities often managed in the community. Awareness of these predictors can help clinicians to identify which older adults are at greater risk of admission for ADRs and, therefore, who might benefit from closer monitoring.
Mucociliary function, ciliary ultrastructure, and ciliary orientation in Young's syndrome.
Authors: R de Iongh, A Ing, J Rutland
Journal: Thorax (1992)

BACKGROUND: Mucociliary clearance is impaired in patients with Young9s syndrome (obstructive azoospermia with recurrent sinobronchial disease), cystic fibrosis, and primary ciliary dyskinesia. No defect of cilia or mucus has been detected in Young9s syndrome. METHODS: Ciliary function and ultrastructure, including ciliary orientation, were studied quantitatively in 20 patients with Young9s syndrome and 20 normal subjects to determine the incidences of ciliary defects. Nasal ciliated epithelium was obtained from each subject and used for measurement of ciliary beat frequency and ultrastructural analyses. Ciliary orientation was determined by measuring ciliary deviation in electron micrographs; ciliary deviation is a measure of the relative orientation of cilia in relation to each other in which high values indicate ciliary disorientation. RESULTS: Ciliary beat frequency and the incidence of microtubular defects and numbers of dynein arms did not differ between patients with Young9s syndrome and control subjects. In patients with Young9s syndrome basal ciliary deviation (16.0 degrees) was similar to that in control subjects (14.1 degrees), but at the ciliary tip ciliary deviation (21.9 degrees) was greater than in healthy subjects (14.5 degrees). CONCLUSION: The relative disorientation of the distal ciliary axoneme in patients with Young9s syndrome compared with normal subjects may be due to a structural defect but is more likely to be a consequence of abnormal mucus.
Fusidic acid in dermatology
Authors: None Wilkinson
Journal: British Journal of Dermatology (1998)

Fusidic acid is an antibiotic that belongs to a group of its own, the fusidanes. The molecule has a steroid‐like structure but does not possess any steroid activity. The structure is thought to be responsible for the steroid‐like high penetration, and for the fact that no cross‐resistance or cross‐allergy has been seen with other antibiotics in routine clinical use. The anti‐microbial activity of fusidic acid is specifically aimed at the most common skin pathogens, including Staphylococcus aureus, towards which it is one of the most potent antibiotics. The place of fusidic acid in dermatology is in the treatment of mild to moderately severe skin and soft‐tissue infections, e.g. impetigo, folicullitis, erythrasma, furunculosis, abscesses and infected traumatic wounds, whereas it is of less use in conditions such as hidradenitis suppurativa, chronic leg ulcers, burns and pressure sores. The topical combinations of fusidic acid with either betamethasone or hydrocortisone are extremely useful in the treatment of atopic dermatitis/eczema whenever staphylococcal/secondary infection is suspected, and in more persistent cases of eczema where staphylococcal superantigen may be playing an important exacerbating role.
Chest Pain in Cardiac-Transplant Recipients
Authors: Randall P. Stark, Andrew L. McGinn, Robert F. Wilson
Journal: New England Journal of Medicine (1991)

ALTHOUGH coronary artery disease develops within three years of heart transplantation in up to 40 percent of transplant recipients,1 , 2 chest pain late after cardiac transplantation is usually dismissed as being noncardiac because it has been assumed that the transplanted heart is permanently denervated. The presumption that the donor heart remains denervated in humans is based primarily on the lack of appropriate neural reflex—mediated changes in the heart rate.3 , 4 That reinnervation would not occur is surprising, because there is extensive evidence of sympathetic reinnervation after cardiac transplantation in nearly all animal models.5 6 7 8 In the transplanted heart, sympathetic nerves are severed from . . .
Relationship of Symptom-Onset-to-Balloon Time and Door-to-Balloon Time With Mortality in Patients Undergoing Angioplasty for Acute Myocardial Infarction
Authors: Christopher P. Cannon
Journal: JAMA (2000)

ContextRapid time to treatment with thrombolytic therapy is associated with lower mortality in patients with acute myocardial infarction (MI). However, data on time to primary angioplasty and its relationship to mortality are inconclusive.ObjectiveTo test the hypothesis that more rapid time to reperfusion results in lower mortality in the strategy of primary angioplasty.DesignProspective observational study of data collected from the Second National Registry of Myocardial Infarction between June 1994 and March 1998.SettingA total of 661 community and tertiary care hospitals in the United States.SubjectsA cohort of 27,080 consecutive patients with acute MI associated with ST-segment elevation or left bundle-branch block who were treated with primary angioplasty.Main Outcome MeasureIn-hospital mortality, compared by time from acute MI symptom onset to first balloon inflation and by time from hospital arrival to first balloon inflation (door-to-balloon time).ResultsUsing a multivariate logistic regression model, the adjusted odds of in-hospital mortality did not increase significantly with increasing delay from MI symptom onset to first balloon inflation. However, for door-to-balloon time (median time 1 hour 56 minutes), the adjusted odds of mortality were significantly increased by 41% to 62% for patients with door-to-balloon times longer than 2 hours (for 121-150 minutes: odds ratio [OR], 1.41; 95% confidence interval [CI], 1.08-1.84; P=.01; for 151-180 minutes: OR, 1.62; 95% CI, 1.23-2.14; P&lt;.001; and for &gt;180 minutes: OR, 1.61; 95% CI, 1.25-2.08; P&lt;.001).ConclusionsThe relationship in our study between increased mortality and delay in door-to-balloon time longer than 2 hours (present in nearly 50% of this cohort) suggests that physicians and health care systems should work to minimize door-to-balloon times and that door-to-balloon time should be considered when choosing a reperfusion strategy. Door-to-balloon time also appears to be a valid quality-of-care indicator.
Paradigm of Genetic Mosaicism and Lone Atrial Fibrillation
Authors: Isabelle L. Thibodeau, Ji Xu, Qiuju Li, Gele Liu, Khanh Lam, John P. Veinot, David H. Birnie, Douglas L. Jones, Andrew D. Krahn, Robert Lemery, Bruce J. Nicholson, Michael H. Gollob
Journal: Circulation (2010)

Background— Atrial fibrillation (AF) is the most common sustained arrhythmia observed in otherwise healthy individuals. Most lone AF cases are nonfamilial, leading to the assumption that a primary genetic origin is unlikely. In this study, we provide data supporting a novel paradigm that atrial tissue–specific genetic defects may be associated with sporadic cases of lone AF. Methods and Results— We sequenced the entire coding region of the connexin 43 (Cx43) gene ( GJA1 ) from atrial tissue and lymphocytes of 10 unrelated subjects with nonfamilial, lone AF who had undergone surgical pulmonary vein isolation. In the atrial tissue of 1 patient, we identified a novel frameshift mutation caused by a single nucleotide deletion (c.932delC) that predicted 36 aberrant amino acids followed by a premature stop codon, leading to truncation of the C-terminal domain of Cx43. The mutation was absent from the lymphocyte DNA of the patient, indicating genetic mosaicism. Protein trafficking studies demonstrated intracellular retention of the mutant protein and a dominant-negative effect on gap junction formation of both wild-type Cx43 and Cx40. Electrophysiological studies revealed no electrical coupling of cells expressing the mutant protein alone and significant reductions in coupling when coexpressed with wild-type connexins. Conclusions— This study reports atrial tissue genetic mosaicism of a novel loss-of-function Cx43 mutation associated with lone AF. These findings implicate somatic genetic defects of Cx43 as a potential cause of AF and support the paradigm that sporadic, nonfamilial cases of lone AF may arise from genetic mosaicism that creates heterogeneous coupling patterns, predisposing the tissue to reentrant arrhythmias.
Medical insurance crisis hits Australia's surgeons
Authors: C. Zinn
Journal: BMJ (2002)

Up to 60% of Australia's surgeons are threatening to retire early and almost a third of trainees are planning to quit because of rising medical indemnity costs, a survey has found.

In the latest fallout from the continuing insurance crisis, the Royal Australasian College of Surgeons, which conducted the poll, warned that the mass exodus of surgeons would be catastrophic for …
Changes in the metabolic clearance of vasopressin and in plasma vasopressinase throughout human pregnancy.
Authors: J M Davison, E A Sheills, W M Barron, A G Robinson, M D Lindheimer
Journal: Journal of Clinical Investigation (1989)

Metabolic clearance rates (MCR) of arginine vasopressin (AVP) were measured serially in five women starting before conception, during gestational weeks 7-8 (early), 22-24 (middle), and 36-38 (late pregnancy), and again 10-12 wk postpartum. Hormonal disposal rates were determined after water loading to suppress endogenous AVP release using a constant infusion method designed to achieve three different steady-state concentrations of plasma AVP (PAVP) on each test occasion. Dose schedules were altered in mid- and late pregnancy to obtain comparable AVP levels at each stage of the protocol. Prehydration decreased plasma osmolality sufficiently to suppress AVP release, as circulating AVP-neurophysin measured serially in three of the women was undetectable. The MCR of AVP was similar before conception (0.75 +/- 0.31, 0.79 +/- 0.34, and 0.76 +/- 0.28 liters/min at PAVP of 2.6 +/- 1.9, 4.7 +/- 2.4, and 8.3 +/- 3.9 pg/ml), in early pregnancy (0.89 +/- 0.34, 0.97 +/- 0.04, and 0.95 +/- 0.40 liters/min at PAVP of 2.2 +/- 2.1, 3.9 +/- 3.2, and 7.9 +/- 3.4 pg/ml), and postpartum (0.70 +/- 0.21, 0.69 +/- 0.24, and 0.75 +/- 0.20 liters/min at PAVP 3.5 +/- 1.8, 5.1 +/- 3.7, and 9.1 +/- 4.2 pg/ml). Values at mid-pregnancy (2.8 +/- 1.3, 3.0 +/- 1.2, and 2.7 +/- 1.2 liters/min at PAVP 2.3 +/- 2.2, 4.0 +/- 3.6, and 7.7 +/- 3.9 pg/ml) and late pregnancy (3.2 +/- 1.4, 3.3 +/- 1.4, and 2.9 +/- 1.2 liters/min at PAVP 1.9 +/- 2.0, 3.8 +/- 2.6, and 7.4 +/- 4.1 pg/ml) increased 3-4-fold (all P less than 0.01). Plasma vasopressinase, undetectable at 7-8 gestational wk, increased markedly by mid- and slightly more by late gestation. Finally, relationships between PAVP and urine osmolality were similar before, during, and after pregnancy. We conclude that marked increments in the MCR of AVP occur between gestational weeks 7 and 8 and mid-pregnancy, which parallel the period of greatest rise in both trophoblastic mass and plasma vasopressinase. There was no evidence of a renal resistance to AVP during gestation.