tbuckley/cabot-search huggingface dataset:
Progress and Problems in the Fight against AIDS
Authors: Bernard Hirschel, Patrick Francioli
Journal: New England Journal of Medicine (1998)

In this issue of the Journal, Palella et al. provide evidence of a massive decrease in morbidity and mortality related to human immunodeficiency virus (HIV) infection.1 Among 1255 study participants who had at least one CD4+ cell count of fewer than 100 cells per cubic millimeter before enrollment, deaths decreased by 75 percent (from 35.1 to 8.8 per 100 person-years) between early 1994 and mid-1997, and the incidence of AIDS-defining diseases decreased by 73 percent (from approximately 50 to 13.3 per 100 person-years). During this period, progressively more intense antiretroviral therapy was introduced into clinical practice. These improvements occurred not . . .
Fallopian Tube Surgery for Reversal of Sterilization
Authors: G. F. J. Williams
Journal: BMJ (1973)

Of 16 consecutive cases of previous sterilization treated by tubal surgery fifteen women tested had patent Fallopian tubes. Over 18 months since operation there were four full-term pregnancies and two abortions among 11 patients. At interview with the patient it is important to emphasize that reconstruction of the tubes is a major operation and carries an increased subsequent hazard of ectopic pregnancy.
Pathogenesis of hemangioma
Authors: Douglas A. Marchuk
Journal: Journal of Clinical Investigation (2001)

Hemangioma is the most common tumor of any kind seen in infancy. It is also, perhaps, the least understood. This stems in part from a long history of confusing nomenclature for vascular anomalies that employed classification schemes based on superficial descriptions of the lesions. The first major step toward clarifying this nomenclatural morass was made by Mulliken and colleagues (1, 2), who employed a biological classification scheme based on the differing clinical courses and endothelial proliferative activity of hemangiomas versus malformations. Hemangiomas, often called infantile or juvenile hemangiomas for clarity, are benign tumors that exhibit an early and rapid proliferation phase during the first year of life characterized by endothelial and pericytic hyperplasia, followed by a slower but steady involution phase that may last for years. This basic scheme of histopathological classification has been refined by immunohistochemical characterization of hemangioma in each of the phases (3). Nonetheless, the pathogenesis of hemangioma is still not understood. Although growth factors and hormonal and mechanical influences have been postulated to affect the abnormal proliferation of endothelial cells in hemangioma, the primary, causative defect in hemangiogenesis remains unknown and no genetic alteration has been implicated.

This dearth of molecular details is striking, considering the growing list of germline mutations in genes causing specific inherited syndromes involving vascular malformations, including hereditary hemorrhagic telangiectasia (4, 5), cutaneous venous malformations (6), cerebral cavernous malformations (7, 8), and hyperkeratotic cutaneous capillary-venous malformation (9). Are we able to investigate hemangioma in a similar manner? Cheung and colleagues (10) compared the concordance of hemangioma in monozygotic versus dizygotic twins and found no evidence of a strong predisposing inherited component. However, Blei and colleagues described six rare families segregating hemangiomas and/or vascular malformations as an autosomal dominant trait with incomplete penetrance (11). This suggested a predisposing mutation in these families segregating the trait. Genetic involvement was bolstered with the genetic mapping of a locus on chromosome 5q for hemangioma/malformation development in these particular families (12), but the gene responsible has yet to be identified. In addition, it is not certain that this gene plays any role in the more common sporadic hemangiomas.

Into this gene-deficient story comes the paper of Boye and colleagues (13) in this issue of the JCI, showing that endothelial cells derived from hemangioma are clonal in origin and demonstrating that they arise from a common precursor cell. Significantly, fibroblast-like cells isolated from these tumors are not clonal, as determined using a well-established assay based on X-chromosome inactivation in females.
The effect of age and emphysematous and fibrotic injury on the re-cellularization of de-cellularized lungs
Authors: Dino Sokocevic, Nicholas R. Bonenfant, Darcy E. Wagner, Zachary D. Borg, Melissa J. Lathrop, Ying Wai Lam, Bin Deng, Michael J. DeSarno, Taka Ashikaga, Roberto Loi, Andrew M. Hoffman, Daniel J. Weiss
Journal: Biomaterials (2013)
Early diagnosis, genetic marker sought for tuberous sclerosis
Authors: Kathryn Simmons
Journal: JAMA (1984)

A recent "Tuberous Sclerosis Research Workshop," held in Cambridge, Massachusetts, under the sponsorship of the National Institute of Neurological and Communicative Disorders and Stroke and the Tuberous Sclerosis Association of America, examined the current state of knowledge about this congenital disorder which frequently results in mental retardation. Workshop participants discussed the controversy over whether diagnostic tests based on the presence of hypomelanotic macules in the skin of newborns are sufficiently reliable to warrant legislated mass screening programs such as the one that will take effect in Massachusetts in June 1986. They also considered the likelihood of developing techniques for the prenatal diagnosis of the disorder in the future.
Cardiac Myosin Binding Protein C
Authors: Emily Flashman, Charles Redwood, Johanna Moolman-Smook, Hugh Watkins
Journal: Circulation Research (2004)

Myosin binding protein-C (MyBP-C) is a thick filament–associated protein localized to the crossbridge-containing C zones of striated muscle sarcomeres. The cardiac isoform is composed of eight immunoglobulin I–like domains and three fibronectin 3–like domains and is known to be a physiological substrate of cAMP-dependent protein kinase. MyBP-C contributes to thick filament structure via interactions at its C-terminus with the light meromyosin section of the myosin rod and with titin. The protein also has a role in the regulation of contraction, due to the binding of its N-terminus to the subfragment-2 portion of myosin, which reduces actomyosin ATPase activity; phosphorylation abolishes this interaction, resulting in release of the “brake” on crossbridge cycling. Several structural models of the interaction of MyBP-C with myosin have been proposed, although its precise arrangement on the thick filament remains to be elucidated. Mutations in the gene encoding cardiac MyBP-C are a common cause of hypertrophic cardiomyopathy, and this has led to increased interest in the protein’s function. Investigation of disease-causing mutations in domains with unknown function has led to further insights into the mechanism of cMyBP-C action. This Review aims to collate the published data on those aspects of MyBP-C that are well characterized and to consider new and emerging data that further define its structural and regulatory roles and its arrangement in the sarcomere. We also speculate on the mechanisms by which hypertrophic cardiomyopathy–causing truncation and missense mutations affect the normal functioning of the sarcomere.
New US rules ban aggressive debt collection by charitable hospitals
Authors: M. McCarthy
Journal: BMJ (2015)

Charitable hospitals that engage in aggressive billing and debt collection practices can lose their tax exempt status under final rules announced by the US Department of the Treasury on 29 December. The rules1 were mandated by a provision of the 2010 Affordable Care Act.

More than half of US hospitals are nonprofits which, as charitable organizations, qualify for exemptions from income, property, and sales taxes with the understanding that they will …
Nestin expression in the kidney with an obstructed ureter
Authors: T. Sakairi, K. Hiromura, S. Yamashita, S. Takeuchi, M. Tomioka, H. Ideura, A. Maeshima, Y. Kaneko, T. Kuroiwa, M. Nangaku, T. Takeuchi, Y. Nojima
Journal: Kidney International (2007)
Effects of Different Types of Exercise Training Followed by Detraining on Endothelium-Dependent Dilation in Patients With Recent Myocardial Infarction
Authors: M. Vona, G.M. Codeluppi, T. Iannino, E. Ferrari, J. Bogousslavsky, L.K. von Segesser
Journal: Circulation (2009)

Background— In coronary artery disease, exercise training (ET) is associated with an improvement in endothelial function, but little is known about the relative effect of different types of training. The purpose of this study was to prospectively evaluate the effect of different types of ET on endothelial function in 209 patients after a first recent acute myocardial infarction. Methods and Results— Endothelial function was evaluated before and after 4 weeks of different types of ET and after 1 month of detraining by measuring flow-mediated dilation and von Willebrand factor levels at baseline and after ET. Patients were randomized into 4 groups: group 1, aerobic ET (n=52); group 2, resistance training (n=54); group 3, resistance plus aerobic training (n=53); and group 4, no training (n=50). At baseline, flow-mediated dilation was 4.5±2.6% in group 1, 4.01±1.6% in group 2, 4.4±4% in group 3, and 4.3±2.3% in group 4 ( P =NS). After ET, flow-mediated dilation increased to 9.9±2.5% in group 1, 10.1±2.6% in group 2, and 10.8±3% in group 3 ( P &lt;0.01 versus baseline for all groups); it also increased in group 4 but to a much lesser extent (to 5.1±2.5%; P &lt;0.01 versus trained groups). The von Willebrand factor level after ET decreased by 16% ( P &lt;0.01) similarly in groups 1, 2, and 3 but remained unchanged in group 4. Detraining returned flow-mediated dilation to baseline levels ( P &lt;0.01 versus posttraining). Conclusion— In patients with recent acute myocardial infarction, ET was associated with improved endothelial function independently of the type of training, but this effect disappeared after 1 month of detraining.
Dietary boron, brain function, and cognitive performance.
Authors: J G Penland
Journal: Environmental Health Perspectives (1994)

Although the trace element boron has yet to be recognized as an essential nutrient for humans, recent data from animal and human studies suggest that boron may be important for mineral metabolism and membrane function. To investigate further the functional role of boron, brain electrophysiology and cognitive performance were assessed in response to dietary manipulation of boron (approximately 0.25 versus approximately 3.25 mg boron/2000 kcal/day) in three studies with healthy older men and women. Within-subject designs were used to assess functional responses in all studies. Spectral analysis of electroencephalographic data showed effects of dietary boron in two of the three studies. When the low boron intake was compared to the high intake, there was a significant (p < 0.05) increase in the proportion of low-frequency activity, and a decrease in the proportion of higher-frequency activity, an effect often observed in response to general malnutrition and heavy metal toxicity. Performance (e.g., response time) on various cognitive and psychomotor tasks also showed an effect of dietary boron. When contrasted with the high boron intake, low dietary boron resulted in significantly poorer performance (p < 0.05) on tasks emphasizing manual dexterity (studies II and III); eye-hand coordination (study II); attention (all studies); perception (study III); encoding and short-term memory (all studies); and long-term memory (study I). Collectively, the data from these three studies indicate that boron may play a role in human brain function and cognitive performance, and provide additional evidence that boron is an essential nutrient for humans.
Expression of GTPase-deficient Ras inhibits vasopressin signaling in cultured cortical collecting duct cells.
Authors: R Wong, L Heasley, L Ao, T Berl
Journal: Journal of Clinical Investigation (1995)

Cross-talk between signaling pathways is increasingly recognized as integral to cellular function. We investigated whether the mitogen-activated protein kinase (MAPK) pathway alters vasopressin (AVP) stimulation of protein kinase A (PKA) by specifically studying the role of Ras. Mouse cortical collecting duct cells (M-1) were transfected with a cDNA encoding oncogenic Ras. Transfection was confirmed by Western blot analysis and functionally by enhanced basal MAPK activity. When compared with basal MAPK activity of 26.4 +/- 6.6 pmol/mg/min in controls, basal MAPK activity varied widely in Ras-transfected clones from 29.0 +/- 6.6 to 96.6 +/- 13.4 pmol/mg/min. Clones that functionally expressed activated Ras displayed complete abolition of AVP-stimulated PKA activity, whereas those that failed to express elevated basal MAPK activity showed intact AVP-stimulated PKA. The correlation between expression of high basal MAPK activity and inhibition of AVP-induced PKA yielded a correlation coefficient of -0.92 (P = 0.009). Exposure to 10 microM forskolin or 1 microgram/ml cholera toxin resulted in comparable activation of PKA in all clones. We found no correlation between PKC activity of the clones and PKA inhibition. To assess whether the observed effect was due to one known Ras target, cells were transfected with constitutively activated Raf. M-1 cells expressing activated Raf exhibited elevated MAPK activity. The Raf clones showed no impairment of AVP-stimulated PKA activity. We conclude that expression of activated Ras is inhibitory of AVP-induced PKA activation in the M-1 cortical collecting duct cell line at a site proximal to G alpha s protein. The failure of Raf to influence AVP signaling indicates that the action of Ras is through a pathway independent of this Ras target.
Clopidogrel Treatment Prior to Percutaneous Coronary Intervention
Authors: Steven R. Steinhubl, Richard Charnigo
Journal: JAMA (2006)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
THE ADDITIONAL ROLE OF CT IN ASSESSING DISEASES OF THE THYROID
Authors: G. E. Newman, P. M. Silverman, M. Korobkin, J. B. Workman, P. Ram, R. E. Coleman
Journal: Clinical Nuclear Medicine (1982)

Newman, G. E.; Silverman, P. M.; Korobkin, M.; Workman, J. B.; Ram, P.; Coleman, R. E. Author Information
Factor XI gene mutations in factor XI deficient patients of the Czech Republic
Authors: Giancarlo Castaman, Sofia H. Giacomelli, David Habart, Rosanna Asselta, Stefano Duga, Francesco Rodeghiero
Journal: American Journal of Hematology (2008)

Factor XI (FXI) deficiency is an autosomal inherited coagulation disorder characterized by bleeding symptoms mainly associated with injury or surgery. Although most of the FXI gene mutations in Ashkenazi Jews are represented by the Glu117stop or Phe283Leu mutations, considerable genetic heterogeneity has been reported in other populations. We report here the genotypic characterization of four families with severe inherited FXI deficiency from the Czech Republic. Seven different gene mutations (three novel) were identified, thus, excluding the existence of a major founder effect in this population. Interestingly, both Glu117stop and Phe283Leu were detected once, further demonstrating the occurrence of these mutations also outside the Jewish populations. In conclusion, we confirm that FXI deficiency in non-Jewish populations is because of different gene mutations; however, the presence of the Glu117stop and Phe283Leu mutations suggests that genetic testing in FXI-deficient patients can start with these two point mutations.
Abstract LB-346: EGF receptor, Jaks and Stat3 crosstalk promote enhanced colony-forming, motility, migration, and invasive phenotype of cisplatin-resistant ovarian cancer cells
Authors: Peibin Yue, Xiaolei Zhang, David Paladino, Bhaswati Sengupta, Sarfraz Ahmad, Robert W. Holloway, Susan B. Ingersoll, James Turkson
Journal: Cancer Research (2012)

Abstract Majority of the ovarian cancer patients who initially respond to cisplatin therapy develop recurrent and resistant disease that is mechanistically not well understood. To define the biological presentations and the molecular phenotype of cisplatin resistant ovarian cancer, we subjected the sensitive A2780S ovarian cancer line to multiple rounds of cisplatin treatments, followed by recovery and derived the lines, A2780S/CP1 (S/CP1), A2780S/CP3 (S/CP3), and A2780S/CP5 (S/CP5), which are resistant to 1, 3, and 5 μM cisplatin, respectively. In vitro studies show the three resistant lines have increased colony-forming ability and altered morphology consistent with enhanced motility, migration, and invasiveness. The malignant phenotype progresses with increasing resistance and is associated with hyperactive epidermal growth factor receptor (EGFR)/extracellular signal-regulated kinase 1/2 and Janus kinases (Jaks), and aberrant Signal Transducer and Activator of Transcription (Stat) 3 activation. Elevated expression of survivin and vascular endothelial growth factor (VEGF), and enhanced matrix metalloproteinase activities are evident in the resistant cells, together with increased vimentin and snail expression, and E-cadherin downregulation, indicative of epithelial-mesenchymal transition (EMT). The inhibition of EGFR or Stat3 activity in the resistant cells repressed the enhanced colony-forming, motility, and migratory phenotype, downregulated survivin, VEGF and vimentin expression, and sensitized the resistant cells to cisplatin. In vivo studies using intra-peritoneal xenograft models in nude mice revealed the resistant lines have a high tumor incidence and formed small, cisplatin-resistant tumor nodules at several locations on the small-intestine and colon, compared to the sensitive A2780S line that exhibited low tumor incidence and formed exclusively ovarian tumors. Treatment with EGFR or Stat3 inhibitor sensitized the resistant tumor nodules to cisplatin. Studies together indicate hyperactive EGFR and Jak signaling predominantly through the induction of aberrantly-active Stat3 promote EMT during cisplatin resistance development. Collectively, these events serve as critical mediators of the invasive phenotype associated with cisplatin resistant ovarian cancer and hence, are targets for preventing the development of resistance and the recurrent disease during cisplatin therapy in ovarian cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-346. doi:1538-7445.AM2012-LB-346
Immunodominant epitopes on glycoprotein IIb-IIIa recognized by autoreactive T cells in patients with immune thrombocytopenic purpura
Authors: Masataka Kuwana, Junichi Kaburaki, Hidero Kitasato, Miyako Kato, Shinichi Kawai, Yutaka Kawakami, Yasuo Ikeda
Journal: Blood (2001)
Clinically Useful Problem Statement Systems
Authors: Kenneth J. Gorelick
Journal: Annals of Internal Medicine (2000)

Letters4 April 2000Clinically Useful Problem Statement SystemsKenneth J. Gorelick, MDKenneth J. Gorelick, MDBala Cynwyd, PA 19004 (Gorelick)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-132-7-200004040-00017 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Brown and colleagues (1) propose an interesting and useful system to reduce the number of terms needed to enumerate a patient's medical problems. They achieved a 60-fold reduction, from 891 770 problem statements for 74 696 patients to 15 534 “canonical” terms. They suggest that this will simplify physicians' ability to readily lump diseases together, especially when compared with the unwieldy International Classification of Diseases, 9th Revision, Clinical Modification.From this elegantly derived research and billing tool, Dr. Voytovich (2) takes us into the brave new world of the “handoff” of patients from hospitalists to ambulatory care ...References1. Brown SH, Miller RA, Camp HN, Guise DA, Walker HK. Empirical derivation of an electronic clinically useful problem statement system. Ann Intern Med. 1999;131:117-26. LinkGoogle Scholar2. Voytovich AE. Reduction of medical verbiage: fewer words, more meaning [Editorial]. Ann Intern Med. 1999;131:146-7. LinkGoogle Scholar3. Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA, et al . Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992;101:1644-55. CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: Bala Cynwyd, PA 19004 (Gorelick) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoEmpirical Derivation of an Electronic Clinically Useful Problem Statement System Steven H. Brown , Randolph A. Miller , Henry N. Camp , Dario A. Guise , and H. Kenneth Walker Reduction of Medical Verbiage: Fewer Words, More Meaning Anthony E. Voytovich Metrics 4 April 2000Volume 132, Issue 7Page: 592KeywordsClinical trialsComplementary and alternative medicineDrugsHospitalistsInternational Classification of DiseasesPatientsPopulation statisticsResearch designScientistsSoftware tools Issue Published: 4 April 2000 CopyrightCopyright © 2000 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...