St Lukes Roosevelt Hospital Medical Center

New York City, NY, United States

St Lukes Roosevelt Hospital Medical Center

New York City, NY, United States

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Ortega-Gutierrez S.,Columbia University | Ortega-Gutierrez S.,St Lukes Roosevelt Hospital Medical Center | Linares G.,Columbia University | Cunningham A.,Columbia University | And 3 more authors.
Journal of Spinal Disorders and Techniques | Year: 2014

Introduction: Fibrocartilaginous embolism (FCE) is an uncommon cause of myelopathy that should be considered after more common causes have been ruled out.Objective: This article presents a case report of a 50-year-old man with acute myelopathy attributed to FCE and summarizes the clinical features of the disease by analyzing all of the published evidence.Data Sources and Extraction: Two computerized literature searches (MEDLINE-Pubmed, EMBASE, the Cochrane Library) were performed. The search term used was "Fibrocartilaginous embolism." No language restrictions were applied. All articles were evaluated and key data were extracted according to predefined criteria: patient's age, year of publication, localization of the embolism and type of vascular syndrome, clinical outcome, and time to death in the fatal cases.Results: Fifty-two cases (39 biopsy proven and 13 clinically diagnosed) were found in the literature. Median age at presentation was 37 years (interquartile range, 19-53) and 56% were women. Median progression of symptoms was 6 hours (interquartile range, 5-60 h), predominantly affecting the cervical spine (48%) by an arterial embolic source (56%).Conclusions: FCE is an unusual cause of spinal cord and cerebral ischemia with unknown incidence. Implementation of diagnostic imaging techniques and initial management of acute spinal disorders care in intensive care units might increase the incidence of disease antemortem. FCE should be considered in the differential diagnosis of ischemic spinal cord injury when no other causes can be identified and especially when the onset is progressive over several hours. Copyright © 2014 by Lippincott Williams & Wilkins.


Kissileff H.R.,St Lukes Roosevelt Hospital Medical Center | Kissileff H.R.,Columbia University | Thornton J.C.,St Lukes Roosevelt Hospital Medical Center | Torres M.I.,St Lukes Roosevelt Hospital Medical Center | And 5 more authors.
American Journal of Clinical Nutrition | Year: 2012

Background: Individuals who are weight-reduced or leptin deficient have a lower energy expenditure coupled with higher hunger and disinhibition and/or delayed satiation compared with never-weight-reduced control subjects. Because exogenous leptin inhibits feeding in congenitally leptin-deficient humans, reduced leptin signaling may reduce the expression of feeding inhibition in humans. Objective: The objective was to test the hypothesis that reduced leptin signaling may reduce the expression of feeding inhibition (ie, blunt satiation) in humans by examining the effects of leptin repletion on feeding behavior after weight loss. Design: Ten obese humans (4 men, 6 women) were studied as inpatients while they received a weight-maintaining liquid-formula diet. Satiation was studied by measuring intake and ratings of appetite- related dispositions 3 h after ingestion of 300 kcal of the liquid-formula diet. The subjects were studied at each of 3 time periods: 1) while they maintained their usual weight (W tinitial) and then after weight reduction and stabilization at 10% below initial weight and while they received 5 wk of either 2) twice-daily injections of placebo (Wt- 10%placebo) or 3) "replacement doses" of leptin (Wt-10%leptin) in a single-blind crossover design with a 2-wk washout period between treatments. Energy expenditure was also measured at each study period. Results: Both energy expenditure and visual analog scale ratings that reflect satiation were significantly lower at Wt- 10%placebo than at W tinitial and Wt- 10%leptin. Conclusion: The results are consistent with the hypothesis that the absence of leptin signaling after weight loss may blunt the expression of feeding inhibition in humans. © 2012 American Society for Nutrition.


Rosenbaum M.,Columbia University | Kissileff H.R.,Columbia University | Kissileff H.R.,St Lukes Roosevelt Hospital Medical Center | Mayer L.E.S.,Columbia University | And 2 more authors.
Brain Research | Year: 2010

Almost anyone who has ever lost weight can attest that it is harder to sustain weight loss than to lose weight. Maintenance of a 10% or greater reduced body weight is accompanied by decreases in energy expenditure to levels significantly below what is predicted solely on the basis of weight and body composition changes. This disproportionate decline in energy expenditure would not be sufficient to account for the over 80% recidivism rate to pre-weight loss levels of body fatness after otherwise successful weight reduction if there were a corresponding reduction in energy intake. In fact, reduced body weight maintenance is accompanied by increased energy intake above that required to maintain reduced weight. The failure to reduce energy intake in response to decreased energy output reflects decreased satiation and perception of how much food is eaten and multiple changes in neuronal signaling in response to food which conspire with the decline in energy output to keep body energy stores (fat) above a CNS-defined minimum (threshold). Much of this biological opposition to sustained weight loss is mediated by the adipocyte-derived hormone "leptin." © 2010 Elsevier B.V. All rights reserved.


PubMed | St Lukes Roosevelt Hospital Medical Center
Type: Journal Article | Journal: The American journal of clinical nutrition | Year: 2012

Individuals who are weight-reduced or leptin deficient have a lower energy expenditure coupled with higher hunger and disinhibition and/or delayed satiation compared with never-weight-reduced control subjects. Because exogenous leptin inhibits feeding in congenitally leptin-deficient humans, reduced leptin signaling may reduce the expression of feeding inhibition in humans.The objective was to test the hypothesis that reduced leptin signaling may reduce the expression of feeding inhibition (ie, blunt satiation) in humans by examining the effects of leptin repletion on feeding behavior after weight loss.Ten obese humans (4 men, 6 women) were studied as inpatients while they received a weight-maintaining liquid-formula diet. Satiation was studied by measuring intake and ratings of appetite-related dispositions 3 h after ingestion of 300 kcal of the liquid-formula diet. The subjects were studied at each of 3 time periods: 1) while they maintained their usual weight (Wt(initial)) and then after weight reduction and stabilization at 10% below initial weight and while they received 5 wk of either 2) twice-daily injections of placebo (Wt(-10%placebo)) or 3) replacement doses of leptin (Wt(-10%leptin)) in a single-blind crossover design with a 2-wk washout period between treatments. Energy expenditure was also measured at each study period.Both energy expenditure and visual analog scale ratings that reflect satiation were significantly lower at Wt(-10%placebo) than at Wt(initial) and Wt(-10%leptin).The results are consistent with the hypothesis that the absence of leptin signaling after weight loss may blunt the expression of feeding inhibition in humans.

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