Tufts University

About: Tufts University is a education organization based out in Medford, Massachusetts, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 32800 authors who have published 66881 publications receiving 3451152 citations. The organization is also known as: Tufts College & Universitatis Tuftensis.

Interleukin-1 immunoreactive innervation of the human hypothalamus

Abstract: Interleukin-1 (IL-1) is a cytokine that mediates the acute phase reaction. Many of the actions of IL-1 involve direct effects on the central nervous system. However, IL-1 has not previously been identified as an intrinsic component within the brain, except in glial cells. An antiserum directed against human IL-1 beta was used to stain the human brain immunohistochemically for IL-1 beta-like immunoreactive neural elements. IL-1 beta-immunoreactive fibers were found innervating the key endocrine and autonomic cell groups that control the central components of the acute phase reaction. These results indicate that IL-1 may be an intrinsic neuromodulator in central nervous system pathways that mediate various metabolic functions of the acute phase reaction, including the body temperature changes that produce the febrile response.

Efficacy and Safety of Monoclonal Antibody to Human Tumor Necrosis Factor α in Patients With Sepsis Syndrome: A Randomized, Controlled, Double-blind, Multicenter Clinical Trial

Abstract: Objective. —To evaluate the efficacy and safety of anti—tumor necrosis factor α monoclonal antibody (TNF-α MAb) in the treatment of patients with sepsis syndrome. Design. —Randomized, prospective, multicenter, double-blind, placebo-controlled clinical trial. Setting. —A total of 31 hospitals in the United States and Canada. Patients. —There were 994 patients with sepsis syndrome enrolled in this clinical trial, and 971 patients were infused with the study drug. Intervention. —Patients were prospectively stratified into shock or nonshock groups and then randomized to receive a single infusion of 15 mg/kg of TNF-α MAb, 7.5 mg/kg of TNF-α MAb, or placebo. Patients received standard aggressive medical and surgical care during the 28-day postinfusion period. Outcome Measure. —Twenty-eight-day all-cause mortality. Results. —The distribution of variables describing demographics, organ system dysfunction or failure, preinfusion Acute Physiology and Chronic Health Evaluation II score, number of organs failing at baseline, initial sites of infection, infecting microorganisms, antimicrobials used, and initial invasive procedures was similar among patients in the TNF-α MAb and placebo treatment arms. Among all infused patients, there was no difference in all-cause mortality in patients who received placebo as compared with those who received TNF-α MAb. In septic patients with shock (n=478), there was a trend toward a reduction in all-cause mortality, which was most evident 3 days after infusion: 25 of 162 patients treated with 15 mg/kg of TNF-α MAb died, 22 of 156 patients treated with 7.5 mg/kg of TNF-α MAb died, and 44 of 160 patients in the placebo group died (15 mg/kg: 44% reduction vs placebo, P =.01; 7.5 mg/kg: 48.7% reduction vs placebo, P =.004). At day 28, the reduction in mortality for shock patients was not significant for either dose of TNF-α MAb relative to placebo (15 mg/kg, 61 deaths among 162 patients [37.7% mortality]; 7.5 mg/kg, 59 deaths among 156 patients [37.8% mortality]; placebo, 73 deaths among 160 patients [45.6% mortality]; P =.20 for 7.5 mg/kg and P =.15 for 15 mg/kg). Serious adverse events were reported in 4.6% of all infused patients. No immediate hypersensitivity allergic reactions due to TNF-α MAb were reported. Serum sickness—like reactions were seen in 2.5% of patients receiving TNF-α MAb. Conclusions. —There was no decrease in mortality between placebo and TNF-α MAb in all infused patients. In septic shock patients who received TNF-α MAb, a significant reduction in mortality was present 3 days after infusion. Although a trend toward reduced mortality continued at 28 days following treatment with TNF-α MAb, the difference in mortality among shock patients treated with placebo or TNF-α MAb was not significant. ( JAMA . 1995;273:934-941)