1,312 research outputs found

    LYMPHOCYTE MEMBRANE DYNAMICS : METABOLIC RELEASE OF CELL SURFACE PROTEINS

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    Cell surface proteins of normal and neoplastic lymphocytes were labeled with iodide-125I by lactoperoxidase-catalyzed iodination. Incubation of 125I-labeled iodide cells in vitro resulted in the release of iodinated surface proteins at a rapid rate which was dependent on cellular respiration and protein synthesis. Comparisons by disc electrophoresis showed a marked similarity between urea-soluble surface proteins extracted from iodinated cells and iodinated material released by the cells during in vitro incubation. The rate of release of cell surface proteins from thymus cells was three times faster than that of spleen cells or bone marrow-derived thoracic duct lymphocytes. In addition, different proteins were released at different rates as evidenced by the rate of release of 125I of rabbit anti-mouse immunoglobulin specifically bound to mouse spleen cells and comparisons by disc electrophoresis of urea-soluble iodinated surface proteins extracted from cells before and after incubation. The results suggest that a dynamic state exists at the cell surface. The possible role of the release of cell surface proteins in cell regulation and communication is discussed

    Sarcoidosis Diagnosed After September 11, 2001, Among Adults Exposed to the World Trade Center Disaster

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    Objective: Explore relationships between World Trade Center (WTC) exposures and sarcoidosis. Methods: Sarcoidosis has been reported after exposure to the WTC disaster. We ascertained biopsy-proven post-9/11 sarcoidosis among WTC Health Registry enrollees. Cases diagnosed after Registry enrollment were included in a nested case–control study. Controls were matched to cases on age, sex, race or ethnicity, and eligibility group (eg, rescue or recovery worker). Results: We identified 43 cases of post-9/11 sarcoidosis. Twenty-eight incident cases and 109 controls were included in the case–control analysis. Working on the WTC debris pile was associated with sarcoidosis (odds ratio 9.1, 95% confidence interval 1.1 to 74.0), but WTC dust cloud exposure was not (odds ratio 1.0, 95% confidence interval 0.4 to 2.8). Conclusions: Working on the WTC debris pile was associated with an elevated risk of post-9/11 sarcoidosis. Occupationally exposed workers may be at increased risk

    Effect of asthma and PTSD on persistence and onset of gastroesophageal reflux symptoms among adults exposed to the September 11, 2001, terrorist attacks

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    Background: Little is known about the direction of causality among asthma, posttraumatic stress disorder (PTSD), and onset of gastroesophageal reflux symptoms (GERS) after exposure to the 9/11/2001 World Trade Center (WTC) disaster. Methods: Using data from the WTC Health Registry, we investigated the effects of early diagnosed post-9/11 asthma and PTSD on the late onset and persistence of GERS using log-binomial regression, and examined whether PTSD mediated the asthma-GERS association using structural equation modeling. Results: Of 29,406 enrollees, 23% reported GERS at follow-up in 2011–2012. Early post-9/11 asthma and PTSD were each independently associated with both the persistence of GERS that was present at baseline and the development of GERS in persons without a prior history. PTSD mediated the association between early post-9/11 asthma and late-onset GERS. Conclusions: Clinicians should assess patients with post-9/11 GERS for comorbid asthma and PTSD, and plan medical care for these conditions in an integrated fashion

    Immune Amplification of Murine CD8+ Suppressor T Cells Induced via An Immune-Privileged Site: Quantifying Suppressor T Cells Functionally

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    BACKGROUND: CD8(+) suppressor T cells exert antigen-specific suppression of the expression of hypersensitivity by activated T cells. Therefore, CD8(+) suppressor T cells serve a major regulatory role for the control of active immunity. Accordingly, the number and/or activity of CD8(+) suppressor T cells should be influenced by an immune response to the antigen. To test this hypothesis we used an adoptive transfer assay that measures the suppression of the expression of delayed-type hypersensitivity (DTH) by CD8(+) suppressor T cells to quantify the antigen-specific suppression of DTH by these suppressor T cells. METHODS: Suppressor T cells were induced in the spleens of mice by the injection of antigen into the anterior chamber of an eye. Following this injection, the mice were immunized by the same antigen injected into the anterior chamber. Spleen cells recovered from these mice (AC-SPL cells) were titrated in an adoptive transfer assay to determine the number of AC-SPL cells required to effect a 50% reduction of antigen-induced swelling (Sw50) in the footpad of immunized mice challenged by antigen. RESULTS: Suppression of the expression of DTH is proportional to the number of AC-SPL cells injected into the site challenged by antigen. The number of AC-SPL cells required for a 50% reduction in DTH-induced swelling is reduced by injecting a cell population enriched for CD8(+) AC-SPL cells. Immunizing the mice receiving intracameral antigen to the same antigen decreases the RSw50 of AC-SPL cells required to inhibit the expression of DTH. CONCLUSIONS: The results provide the first quantitative demonstration that the numbers of antigen-specific splenic CD8(+) suppressor T cells are specifically amplified by antigen during an immune response

    LYMPHOCYTE MEMBRANE DYNAMICS

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    Factors associated with poor control of 9/11-related asthma 10–11 years after the 2001 World Trade Center terrorist attacks

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    Objective: To identify key factors associated with poor asthma control among adults in the World Trade Center (WTC) Health Registry, a longitudinal study of rescue/recovery workers and community members who were directly exposed to the 2001 WTC terrorist attacks and their aftermath. Methods: We studied incident asthma diagnosed by a physician from 12 September 2001 through 31 December 2003 among participants aged ≥18 on 11 September 2001, as reported on an enrollment (2003–2004) or follow-up questionnaire. Based on modified National Asthma Education and Prevention Program criteria, asthma was considered controlled, poorly-controlled, or very poorly-controlled at the time of a 2011–2012 follow-up questionnaire. Probable post-traumatic stress disorder, depression, and generalized anxiety disorder were defined using validated scales. Self-reported gastroesophageal reflux symptoms (GERS) and obstructive sleep apnea (OSA) were obtained from questionnaire responses. Multinomial logistic regression was used to examine factors associated with poor or very poor asthma control. Results: Among 2445 participants, 33.7% had poorly-controlled symptoms and 34.6% had very poorly-controlled symptoms in 2011–2012. Accounting for factors including age, education, body mass index, and smoking, there was a dose–response relationship between the number of mental health conditions and poorer asthma control. Participants with three mental health conditions had five times the odds of poor control and 13 times the odds of very poor control compared to participants without mental health comorbidities. GERS and OSA were significantly associated with poor or very poor control. Conclusions: Rates of poor asthma control were very high in this group with post-9/11 diagnosed asthma. Comprehensive care of 9/11-related asthma should include management of mental and physical health comorbidities

    Cardiovascular Disease Hospitalizations in Relation to Exposure to the September 11, 2001 World Trade Center Disaster and Posttraumatic Stress Disorder

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    Background-—A cohort study found that 9/11-related environmental exposures and posttraumatic stress disorder increased self-reported cardiovascular disease risk. We attempted to replicate these findings using objectively defined cardiovascular disease hospitalizations in the same cohort. Methods and Results-—Data for adult World Trade Center Health Registry enrollees residing in New York State on enrollment and no cardiovascular disease history (n=46 346) were linked to a New York State hospital discharge–reporting system. Follow-up began at Registry enrollment (2003–2004) and ended at the first cerebrovascular or heart disease (HD) hospitalization, death, or December 31, 2010, whichever was earliest. We used proportional hazards models to estimate adjusted hazard ratios (AHRs) for HD (n=1151) and cerebrovascular disease (n=284) hospitalization during 302 742 person-years of observation (mean follow-up, 6.5 years per person), accounting for other factors including age, race/ethnicity, smoking, and diabetes. An elevated risk of HD hospitalization was observed among women (AHR 1.32, 95% CI 1.01 to 1.71) but not men (AHR 1.16, 95% CI 0.97 to 1.40) with posttraumatic stress disorder at enrollment. A high overall level of World Trade Center rescue and recovery–related exposure was associated with an elevated HD hospitalization risk in men (AHR 1.82, 95% CI 1.06 to 3.13; P for trend=0.05), but findings in women were inconclusive (AHR 3.29, 95% CI 0.85 to 12.69; P for trend=0.09). Similar associations were observed specifically with coronary artery disease hospitalization. Posttraumatic stress disorder increased the cerebrovascular disease hospitalization risk in men but not in women. Conclusions-—9/11-related exposures and posttraumatic stress disorder appeared to increase the risk of subsequent hospitalization for HD and cerebrovascular disease. This is consistent with findings based on self-reported outcomes

    Prospects for radical emissions reduction through behaviour and lifestyle change

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    Over the past two decades, scholars and practitioners across the social sciences, in policy and beyond have proposed, trialled and developed a wide range of theoretical and practical approaches designed to bring about changes in behaviours and lifestyles that contribute to climate change. With the exception of the establishment of a small number of iconic behaviours such as recycling, it has however proved extremely difficult to bring about meaningful transformations in personal greenhouse gas emissions at either the individual or societal level, with multiple reviews now pointing to the limited efficacy of current approaches. We argue that the majority of approaches designed to achieve mitigation have been constrained by the need to operate within prevailing social scientific, economic and political orthodoxies which have precluded the possibility of non-marginal change. In this paper we ask what a truly radical approach to reducing personal emissions would look like from social science perspectives which challenge the unstated assumptions severely limiting action to date, and which explore new alternatives for change. We emphasise the difficulties likely to impede the instituting of genuinely radical societal change regarding climate change mitigation, whilst proposing ways that the ground could be prepared for such a transformation to take place
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