Faculty Bibliography
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99
Surgical interactive multimedia modules: A novel, non-browser based architecture for medical education
Contemporary medical education faces new challenges as the climate of the health care delivery system transforms. Diminished length-of-stay and continuity-of-care have radically altered the way medical students are exposed to and learn about illness. These educational challenges are particularly pronounced in the teaching of surgery. We developed a multimedia application, Surgical Interactive Multimedia Modules (SIMM), to utilize rich media objects and high-resolution video to overcome modern didactic challenges. The SIMM client was created using Macromedia Director MX and communicates using XML with an Oracle database containing the rich-media educational objects. The SIMMs integrate digital video, 3-D models, self-assessment tools, and current medical evidence to generate a dynamic learning environment encompassing core surgery topics. Students can access SIMM modules either via a high-speed network connection or by using a DVD. The interface was designed to focus on a narrative timeline that provided students with a familiar metaphor for interacting with the learning objects. Students on the surgery clerkship are currently using four SIMM modules and feedback indicates that they are regarded as compelling and useful educational tools for learning about complex surgical topics. Future areas of research will address student ability to annotate the learning objects and to maintain a personal repository of medical education resources
SCOPUS:4544385508
ISSN: 1063-7125
CID: 648902
Medical humanities at New York University School of Medicine: an array of rich programs in diverse settings
The New York University School of Medicine has a rich tradition of cultivating programs in medical humanities and professionalism. They are drawn from the departments, centers, students, and faculty in the School of Medicine, have linkages throughout the university, and are interwoven into the fabric and culture of the institution. Some are centrally based in the School of Medicine's deans' office, and others are located in individual departments and receive support from the dean's office. This article describes representative programs for medical students and faculty. Curricular initiatives, the fundamental components of medical students' learning, include a course entitled 'The Physician, Patient, and Society,' a clerkship essay in the Medicine Clerkship, an opportunity for reflection during the medicine clerkship, and a medical humanities elective. In 2002, the Professionalism Initiative was launched to enhance and reflect the values of the medical profession. Its curriculum consists of a series of events that coordinate, particularly, with existing elements of the first-year curriculum (e.g., orientation week, a session during anatomy, a self-assessment workshop, and a peer-assessment workshop). The Master Scholars Program is a group of five, theme-based master societies consisting of faculty and students who share common interests around the society's themes. Programs developed for the societies include colloquia, faculty-led seminars, a mandatory student-mentoring program, and visiting scholars. Finally, the authors describe three high-quality literary publications created at New York University School of Medicine. Each of the initiatives undergoes regular critical examination and reflection that drive future planning
PMID: 14534091
ISSN: 1040-2446
CID: 39038
Ruptured plaques and leaking cells: cost-effectiveness in the diagnosis of acute coronary syndromes [Comment]
PMID: 10610650
ISSN: 0003-4819
CID: 8579
Natriuretic peptides: physiology, therapeutic potential, and risk stratification in ischemic heart disease
BACKGROUND: The natriuretic peptide family consists of four molecules that share significant amino acid sequence homologic characteristics and a looped motif. Atrial natriuretic peptide and brain natriuretic peptide are similar in their ability to promote natriuresis and diuresis, inhibit the renin-angiotensin-aldosterone axis, and act as vasodilators. Understanding of the actions of C-type natriuretic peptide and dendroaspis natriuretic peptide is incomplete, but these two new family members also act as vasodilators. Because of the rapid evolution of information about this peptide family, we reviewed the state of the art with respect to risk stratification and therapeutic ability. METHODS: English-language papers were identified by a MEDLINE database search covering 1966 through 1997 and supplemented with bibliographic references and texts. CONCLUSIONS: The natriuretic peptides are counterregulatory hormones with prognostically important levels. They are similarly upregulated in heart failure and counteract neurohormones that induce vasoconstriction and fluid retention. BNP may be the superior prognosticator for risk stratification after myocardial infarction and is independent of left ventricular ejection fraction. Lastly, experimental trials suggest that administration of exogenous natriuretic peptides or inhibitors of their catabolism to patients with ischemic heart disease may be clinically beneficial
PMID: 9588425
ISSN: 0002-8703
CID: 7806
Wound healing is accelerated by agonists of adenosine A2 (G alpha s-linked) receptors
The complete healing of wounds is the final step in a highly regulated response to injury. Although many of the molecular mediators and cellular events of healing are known, their manipulation for the enhancement and acceleration of wound closure has not proven practical as yet. We and others have established that adenosine is a potent regulator of the inflammatory response, which is a component of wound healing. We now report that ligation of the G alpha s-linked adenosine receptors on the cells of an artificial wound dramatically alters the kinetics of wound closure. Excisional wound closure in normal, healthy mice was significantly accelerated by topical application of the specific A2A receptor agonist CGS-21680 (50% closure by day 2 in A2 receptor antagonists. In rats rendered diabetic (streptozotocin-induced diabetes mellitus) wound healing was impaired as compared to nondiabetic rats; CGS-21680 significantly increased the rate of wound healing in both nondiabetic and diabetic rats. Indeed, the rate of wound healing in the CGS-21680-treated diabetic rats was greater than or equal to that observed in untreated normal rats. These results appear to constitute the first evidence that a small molecule, such as an adenosine receptor agonist, accelerates wound healing in both normal animals and in animals with impaired wound healing
PMCID:2199104
PMID: 9348321
ISSN: 0022-1007
CID: 7954
Randomised double-blind trial of fixed low-dose warfarin with aspirin after myocardial infarction
Background Antiplatelet therapy with aspirin and systematic anticoagulation with warfarin reduce cardiovascular morbidity and mortality after myocardial infarction when given alone. In the Coumadin Aspirin Reinfarction Study (CARS), we aimed to find out whether a combination of low-dose warfarin and low-dose aspirin would give superior results to standard aspirin monotherapy without excessive bleeding risk. Methods We used a randomised double-blind study design. At 293 sites, we randomly assigned 8803 patients who had had myocardial infarction, treatment with 160 mg aspirin, 3 mg warfarin with 80 mg aspirin, or 1 mg warfarin with 80 mg aspirin. Patients took a single tablet daily, and attended for prothrombin time (PT) measurements at weeks 1, 2, 3, 4, 6, and 12, and then every 3 months. Patients were followed up for a maximum of 33 months (median 14 months). Findings The primary event was first occurrence of reinfarction, non-fatal ischaemic stroke, or cardiovascular death. 1-year life-table estimates for the primary event were 8.6% (95% Cl 7.6-9.6) for 160 mg aspirin, 8.4% (7.4-9.4) for 3 mg warfarin with 80 mg aspirin, and 8.8% (7.6-10) for 1 mg warfarin with 80 mg aspirin. Primary comparisons were done with all follow-up data. The relative risk of the primary event for the 160 mg aspirin group compared with the 3 mg warfarin with 80 mg aspirin group was 0.95 (0.81-1.12, p=0.57). For spontaneous major haemorrhage (not procedure related), 1-year life-table estimates were 0.74% (0.43-1.1) in the 160 mg aspirin group and 1.4% (0.94-1.8) in the 3 mg warfarin with 80 mg aspirin group (p=0.014 log rank on follow-up). For the 3382 patients assigned 3 mg warfarin with 80 mg aspirin, the INR results were: at week 1 (n=2985) median 1.51 (IQR 1.23-2.13); at week 4 (n=2701) 1.27 (1.13-1.64); at month 6 (n=2145) 1.19 (1.08-1.44). Interpretation Low, fixed-dose warfarin (1 mg or 3 mg) combined with low-dose aspirin (80 mg) in patients who have had myocardial infarction does not provide clinical benefit beyond that achievable with 160 mg aspirin monotherapy. $$:
ISI:A1997XQ24800008
ISSN: 0140-6736
CID: 130406
Vitamin B6 prevents the endothelial toxicity and rise in intracellular free calcium induced by uremic levels of oxalic acid [Meeting Abstract]
ISI:A1996VN11901292
ISSN: 0009-7322
CID: 52744
The complement activation product C5a stimulates endothelial expression of a novel adhesion protein [Meeting Abstract]
ISI:A1996VH88300333
ISSN: 0004-3591
CID: 52779
Adenosine A(2) receptor occupancy promotes fibroblast and endothelial cell migration and wound healing [Meeting Abstract]
ISI:A1996VH88301701
ISSN: 0004-3591
CID: 52794
The anti-inflammatory mechanism of sulfasalazine is related to adenosine release at inflamed sites
The anti-inflammatory mechanism of sulfasalazine is not well understood. It has recently been shown that sulfasalazine inhibits 5-aminoimidazole-4-carboxamidoribonucleotide (AICAR) transformylase, an enzyme involved in de novo purine biosynthesis. We recently demonstrated that methotrexate promotes intracellular AICAR accumulation, thereby increasing adenosine release and diminishing inflammation, so we tested the hypothesis that sulfasalazine similarly promotes intracellular AICAR accumulation. We studied adenosine release and the state of inflammation in in vitro and in vivo models of the inflammatory process. The adhesion of stimulated neutrophils (FMLP) to endothelial cells preincubated with sulfasalazine was inhibited in a dose-dependent manner. Elimination of extracellular adenosine by addition of adenosine deaminase or inhibition of adenosine by the adenosine A2 receptor antagonist 3,7-dimethyl-1-propargylxanthine (DMPX) completely reversed the anti-inflammatory effect of sulfasalazine (at concentrations <1 microM in this in vitro model. To determine whether this phenomenon was relevant to inhibition of inflammation in vivo, we studied the effect of sulfasalazine (100 mg/kg/day by gastric gavage for 3 days) on leukocyte accumulation in the murine air pouch model of inflammation. Treatment with sulfasalazine markedly decreased the number of leukocytes that accumulated in the inflamed (carrageenan, 2 mg/ml) air pouch. Injection of either adenosine deaminase or DMPX, but not the A1 receptor antagonist 8-cyclopentyl-dipropylxanthine, significantly reversed the anti-inflammatory effects of sulfasalazine treatment. Sulfasalazine increased the exudate adenosine concentration from 127 +/- 64 nM to 869 +/- 47 nM. Moreover, sulfasalazine treatment promoted a marked increase in splenocyte AICAR concentration from 35 +/- 6 to 96 +/- 3 pmols/10(6) splenocytes, which is consistent with the in vitro observation that sulfasalazine inhibits AICAR transformylase. These results indicate that sulfasalazine, like methotrexate, enhances adenosine release at an inflamed site and that adenosine diminishes inflammation via occupancy of A2 receptors on inflammatory cells. Our studies provide evidence that sulfasalazine and methotrexate may be described as a newly recognized family of anti-inflammatory agents that share the property of using adenosine as an antagonist of inflammation
PMID: 8596047
ISSN: 0022-1767
CID: 9818
