Featured Research Studies
Not in the mind but in the cell: increased production of cyclo-oxygenase-2 and inducible NO synthase in chronic fatigue syndrome.
Maes M, Mihaylova I, Kubera M, Bosmans E.
MCare4U Outpatient Clinics, Belgium. Neuro Endocrinol Lett. 2007 Jul 11;28(4).
Chronic fatigue syndrome (CFS) is a medically unexplained disorder, characterized by profound fatigue, infectious, rheumatological and neuropsychiatric symptoms. There is, however, some evidence that CFS is accompanied by signs of increased oxidative stress and inflammation in the peripheral blood. This paper examines the role of the inducible enzymes cyclo-oxygenase (COX-2) and inducible NO synthase (iNOS) in the pathophysiology of CFS. Toward this end we examined the production of COX-2 and iNOS by peripheral blood lymphocytes (PBMC) in 18 CFS patients and 18 normal volunteers and examined the relationships between those inflammatory markers and the severity of illness as measured by means of the FibroFatigue scale and the production of the transcription factor nuclear factor kappa beta (NFkappabeta). We found that the production of COX-2 and iNOS was significantly higher in CFS patients than in normal controls. There were significant and positive intercorrelations between COX-2, iNOS and NFkappabeta and between COX-2 and iNOS, on the one hand, and the severity of illness, on the other. The production of COX-2 and iNOS by PBMCs was significantly related to aches and pain, muscular tension, fatigue, concentration difficulties, failing memory, sadness and a subjective experience of infection. The results suggest that a) an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiology of CFS; b) the inflammatory response in CFS is driven by the transcription factor NFkappabeta; c) symptoms, such as fatigue, pain, cognitive defects and the subjective feeling of infection, indicates the presence of a genuine inflammatory response in CFS patients; and d) CFS patients may be treated with substances that inhibit the production of COX-2 and iNOS.
PMID: 17693978 [PubMed - as supplied by publisher]
Not in the mind of neurasthenic lazybones but in the cell nucleus: patients with chronic fatigue syndrome have increased production of nuclear factor kappa beta.
Maes M, Mihaylova I, Bosmans E. Neuro Endocrinol Lett. 2007 Jul 11;28(4)
MCare4U Outpatient Clinics, Belgium. crc.mh@telenet.be.
There is now some evidence that chronic fatigue syndrome is accompanied by an activation of the inflammatory response system and by increased oxidative and nitrosative stress. Nuclear factor kappa beta (NFkappabeta) is the major upstream, intracellular mechanism which regulates inflammatory and oxidative stress mediators. In order to examine the role of NFkappabeta in the pathophysiology of CFS, this study examines the production of NFkappabeta p50 in unstimulated, 10 ng/mL TNF-alpha (tumor necrosis factor alpha) and 50 ng/mL PMA (phorbolmyristate acetate) stimulated peripheral blood lymphocytes of 18 unmedicated patients with CFS and 18 age-sex matched controls. The unstimulated (F=19.4, df=1/34, p=0.0002), TNF-alpha-(F=14.0, df=1/34, p=0.0009) and PMA-(F=7.9, df=1/34, p=0.008) stimulated production of NFkappabeta were significantly higher in CFS patients than in controls. There were significant and positive correlations between the production of NFkappabeta and the severity of illness as measured with the FibroFatigue scale and with symptoms, such as aches and pain, muscular tension, fatigue, irritability, sadness, and the subjective feeling of infection. The results show that an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiogy of CFS and that previous findings on increased oxidative stress and inflammation in CFS may be attributed to an increased production of NFkappabeta. The results suggest that the symptoms of CFS, such as fatigue, muscular tension, depressive symptoms and the feeling of infection reflect a genuine inflammatory response in those patients. It is suggested that CFS patients should be treated with antioxidants, which inhibit the production of NFkappabeta, such as curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid and omega-3 fatty acids
PMID: 17693979 [PubMed - as supplied by publisher]
Environmental Exposure Assessment, Pollution Sources, and Exposure Agents: A Primer for Pediatric Nursing Professionals
Derek G. Shendell, D.Env, MPH; Ann Pike-Paris, MS, RN. Pediatr Nurs. 2007;33(2):179-182. ©2007 Jannetti Publications, Inc.
Abstract
Children´s environmental health is a growing, interdisciplinary field of diverse professionals and community members working together in policy advocacy, research, health, and environmental interventions and treatment services. Understanding exposure assessment is central to improving children´s health across age, gender, indicators of socioeconomic status, and racial/ethnic groups. In general, children are more susceptible and vulnerable to adverse acute and chronic effects due to acute and chronic exposures to environmental toxicants since they eat more food, drink more fluids, and breathe in more air per unit of body weight than adults; their behaviors and rapid developmental changes also contribute to their risks. By enhancing knowledge and awareness of the basic concepts of human exposure assessment and key details of sources of environmental pollution, pediatric nursing professionals can enhance their practices — clinical and patient education skills — and thus improve daily work in their communities through the promotion of exposure reduction or prevention measures.
Modulation of Human Glutathione S-Transferases by Polyphenon E Intervention
H.-H. Sherry Chow, Iman A. Hakim, Donna R. Vining, James A. Crowell, Margaret E. Tome, James Ranger-Moore, Catherine A. Cordova, Dalia M. Mikhael, Margaret M. Briehl and David S. Alberts. Cancer Epidemiology Biomarkers & Prevention 16, 1662-1666, August 1, 2007. doi: 10.1158/1055-9965.EPI-06-0830.
There is now some evidence that chronic fatigue syndrome is accompanied by an activation of the inflammatory response system and by increased oxidative and nitrosative stress. Nuclear factor kappa beta (NFkappabeta) is the major upstream, intracellular mechanism which regulates inflammatory and oxidative stress mediators. In order to examine the role of NFkappabeta in the pathophysiology of CFS, this study examines the production of NFkappabeta p50 in unstimulated, 10 ng/mL TNF-alpha (tumor necrosis factor alpha) and 50 ng/mL PMA (phorbolmyristate acetate) stimulated peripheral blood lymphocytes of 18 unmedicated patients with CFS and 18 age-sex matched controls. The unstimulated (F=19.4, df=1/34, p=0.0002), TNF-alpha-(F=14.0, df=1/34, p=0.0009) and PMA-(F=7.9, df=1/34, p=0.008) stimulated production of NFkappabeta were significantly higher in CFS patients than in controls. There were significant and positive correlations between the production of NFkappabeta and the severity of illness as measured with the FibroFatigue scale and with symptoms, such as aches and pain, muscular tension, fatigue, irritability, sadness, and the subjective feeling of infection. The results show that an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiogy of CFS and that previous findings on increased oxidative stress and inflammation in CFS may be attributed to an increased production of NFkappabeta. The results suggest that the symptoms of CFS, such as fatigue, muscular tension, depressive symptoms and the feeling of infection reflect a genuine inflammatory response in those patients. It is suggested that CFS patients should be treated with antioxidants, which inhibit the production of NFkappabeta, such as curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid and omega-3 fatty acids.
PMID: 17693979 [PubMed - as supplied by publisher]
Excess dampness and mold growth in homes: an evidence-based review of the aeroirritant effect and its potential causes.
Hope AP, Simon RA. Allergy Asthma Proc. 2007 May-Jun;28(3):262-70
Exposure to fungi produces respiratory disease in humans through both allergic and nonallergic mechanisms. Occupants of homes with excess dampness and mold growth often present to allergists with complaints of aeroirritant symptoms. This review describes the major epidemiological and biological studies evaluating the association of indoor dampness and mold growth with upper respiratory tract symptoms. The preponderance of epidemiological data supports a link between exposure to dampness and excess mold growth and the development of aeroirritant symptoms. In addition, biological and clinical studies evaluating potential causal substances for the aeroirritant effect, notably volatile organic compounds (VOCs), are examined in detail. These studies support the role of VOCs in contributing to the aeroirritant symptoms of occupants of damp and mold-contaminated homes.
