Faculty Bibliography
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100
Coronary artery disease and opioid use
Over the past 20 years, we have observed a paucity of morbidity and mortality due to cardiovascular disease among drug users in a methadone maintenance clinic. The present study investigated whether long-term exposure to opiates or opioids is associated with decreased severity of coronary artery disease (CAD) by comparing 98 decedents with methadone or opiates (M/O) in their blood at autopsy with 97 frequency-matched decedents without M/O. Severe CAD was found significantly less often in M/O-positive decedents (5 of 98) than in M/O-negative decedents (16 of 97). Multiple logistic regression analysis contrasting those with moderate or severe CAD to those with no or mild CAD yielded an odds ratio of 0.43 (95% confidence interval 0.20 to 0.94) for M/O positivity after adjustment for potential confounding. Long-term opiate exposure thus may mitigate CAD severity and its often fatal consequences
PMID: 15135709
ISSN: 0002-9149
CID: 46186
Oxalic acid alters intracellular calcium in endothelial cells
Patients with chronic renal failure (CRF) who undergo hemodialysis experience accelerated atherosclerosis and premature death. While the cause of uremic atherogenesis is unknown, we reported that uremic levels of oxalate, an excretory metabolite, severely inhibit proliferation and migration of human endothelial cells (EC) without affecting other cell types. Since the physical, cellular and molecular events of endothelial injury are clearly established as key factors in the development of plaque, and since inhibition of proliferation and migration would enhance endothelial injury, we have proposed that oxalate is an atherogenic toxin of uremia. In the current study, we used in situ cell counting and total DNA measurement to show that the inhibitory effect of oxalate on proliferation is exclusive to endothelial cells among human cell lines tested (endothelial cells, fibroblasts, aortic smooth muscle cells (SMC), glioblastoma and embryonic kidney cells). Using the fluorescent calcium indicators fura-2 and fluo-3, we correlated the inhibition of proliferation with a prolonged elevation in intracellular free calcium levels. We also demonstrated that all cells tested internalize 14C-oxalic acid. We conclude that plasma oxalate exerts its atherogenic effects by elevating intracellular calcium exclusively in endothelial cells and preventing re-endothelialization
PMID: 15064109
ISSN: 0021-9150
CID: 46112
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
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
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
Effects of amlodipine on glomerular filtration, growth, and injury in experimental hypertension
The objective of this study was to determine whether the calcium antagonist amlodipine could slow the progression of chronic renal disease. We examined the effects of amlodipine on kidney structure and function in two experimental models of hypertension. In the first study, adult, male Munich Wistar rats underwent uninephrectomy and were given weekly injections of desoxycorticosterone and 1% saline for drinking. Rats ingested normal chow or chow containing amlodipine for 8 weeks. The drug reduced systemic blood pressure, but glomerular filtration rate, kidney weight, proteinuria, and morphological evidence of glomerular injury were not affected. In the second study, male spontaneously hypertensive rats underwent uninephrectomy at 5 weeks of age and were followed for 6 months, during which they received no therapy or amlodipine. The drug dose was determined in preliminary studies to be the highest dose not associated with marked growth retardation. Again, although systemic blood pressure was significantly reduced by amlodipine, proteinuria and the prevalence of glomerulosclerosis were similar in amlodipine-treated and control spontaneously hypertensive rats. Micropuncture studies revealed that glomerular pressure remained elevated in amlodipine-treated spontaneously hypertensive rats. Kidney weight and glomerular volume were also similar in amlodipine-treated and control rats. Amlodipine also failed to inhibit platelet aggregation. Therefore, antihypertensive therapy with amlodipine fails to reduce glomerular pressure in spontaneously hypertensive rats as well as glomerular size and injury in spontaneously hypertension rats and desoxycorticosterone-salt hypertension. Although other dihydropyridine calcium antagonists have been found to reduce experimental glomerular injury, these data suggest that amlodipine may not prevent hypertensive nephrosclerosis.
PMID: 8567047
ISSN: 0194-911x
CID: 3893442
Accelerated atherosclerosis in South Asian expatriates living in New York [Meeting Abstract]
ISI:A1996UG20700671
ISSN: 1081-5589
CID: 52967
Evidence for apoptosis in Alzheimer's disease [Meeting Abstract]
ISI:A1996UG20700651
ISSN: 1081-5589
CID: 52966
