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1.  Cardiac manifestations of subarachnoid hemorrhage 
Heart, Lung and Vessels  2013;5(3):168-178.
Cardiac manifestations of intracranial subarachnoid hemorrhage patients include mild electrocardiogram variability, reversible left ventricular dysfunction (Takotsubo), non-ST elevation myocardial infarction, ST-elevation myocardial infarction and cardiac arrest, but their clinical relevance is unclear. The aim of the present study was to categorize the relative frequency of different cardiac abnormalities in patients with subarachnoid hemorrhage and determine the influence of each abnormality on outcome. 
A retrospective review of 617 consecutive patients who presented with non-traumatic aneurysmal subarachnoid hemorrhage at our institution was performed. A cohort of 87 (14.1%) patients who required concomitantly cardiological evaluation was selected for subgroup univariate and multi-variable analysis of radiographic, clinical and cardiac data. 
Cardiac complications included myocardial infarction arrhythmia and congestive heart failure in 47%, 63% and 31% of the patients respectively. The overall mortality of our cohort (23%) was similar to that of national inpatient databases. In our cohort a high World Federation of Neurosurgical Surgeons grading scale and a troponin level >1.0 mcg/L were associated with a 33 times and 10 times higher risk of death respectively.
Among patients suffering from cardiac events at the time of aneurysmal subarachnoid hemorrhage, those with myocardial infarction and in particular those with a troponin level greater than 1.0 mcg/L had a 10 times increased risk of death. 
PMCID: PMC3848675  PMID: 24364008
subarachnoid hemorrhage; SAH; myocardial Infarction; MI; arrhythmia; cardiac outcomes; intracranial aneurysm; Takotsubo stress cardiomyopathy
2.  Relationship between exhaled NO, respiratory symptoms, lung function, bronchial hyperresponsiveness, and blood eosinophilia in school children 
Thorax  2003;58(3):242-245.
Methods: Levels of eNO in a sample of 450 children aged 7–12 years out of a total sample of 2504 school children living in different urban areas near motorways were determined. The aim of this cross-sectional study was to explore the relationship between eNO, impairment of lung function (PEF, FVC, FEV1 and MMEF), bronchial hyperresponsiveness (BHR), and blood eosinophilia in children with and without atopy as assessed by skin prick testing.
Results: Regression analysis showed that wheezing and nasal discharge and conjunctivitis that had occurred during the previous 12 months were positively associated with eNO levels in atopic children (relative increase of 1.48 and 1.41, respectively; p<0.05) but not in non-atopic children. Similarly, BHR and the number of blood eosinophils per ml were positively associated with eNO levels in atopic children (relative increase of 1.55 and 2.29, respectively; p<0.05) but not in non-atopic children. The lung function indices PEF, FVC, FEV1 and MMEF were not associated with eNO levels.
Conclusions: In addition to conventional lung function tests and symptom questionnaires, eNO is a suitable measure of airway inflammation and its application may reinforce the power of epidemiological surveys on respiratory health.
PMCID: PMC1746591  PMID: 12612304
3.  Vaccine-induced antibody responses as parameters of the influence of endogenous and environmental factors. 
Environmental Health Perspectives  2001;109(8):757-764.
In laboratory animals, an adequate way to assess effects of environmental exposures on the immune system is to study effects on antigen-specific immune responses, such as after sensitization to T-cell-dependent antigens. This probably also applies to testing effects in the human population. It has thus been suggested that antibody responses to vaccination might be useful in this context. Vaccination responses may be influenced by a variety of factors other than environmental ones. One factor is the vaccine itself; a second is the vaccination procedure used. In addition, the intrinsic capacity of the recipient to respond to a vaccine, which is determined by sex, genetic factors, and age, is important. Psychological stress, nutrition, and (infectious) diseases are also likely to have an impact. We reviewed the literature on vaccine response. With regard to exogenous factors, there is good evidence that smoking, diet, psychological stress, and certain infectious diseases affect vaccination titers, although it is difficult to determine to what extent. Genetic factors render certain individuals nonresponsive to vaccination. In general, in epidemiologic studies of adverse effects of exposure to agents in the environment in which vaccination titers are used, these additional factors need to be taken into consideration. Provided that these factors are corrected for, a study that shows an association of exposure to a given agent with diminished vaccination responses may indicate suboptimal function of the immune system and clinically relevant diminished immune response. It is quite unlikely that environmental exposures that affect responses to vaccination may in fact abrogate protection to the specific pathogen for which vaccination was performed. Only in those cases where individuals have a poor response to the vaccine may exogenous factors perhaps have a clinically significant influence on resistance to the specific pathogen. An exposure-associated inhibition of a vaccination response may, however, signify a decreased host resistance to pathogens against which no vaccination had been performed.
PMCID: PMC1240401  PMID: 11564609
4.  The role of the immune system in hexachlorobenzene-induced toxicity. 
Environmental Health Perspectives  1999;107(Suppl 5):783-792.
Hexachlorobenzene (HCB) is a persistent environmental pollutant. The toxicity of HCB has been extensively studied after an accidental human poisoning in Turkey and more recently it has been shown that HCB has immunotoxic properties in laboratory animals and probably also in man. Oral exposure of rats to HCB showed stimulatory effects on spleen and lymph node weights and histology, increased serum IgM levels, and an enhancement of several parameters of immune function. Moreover, more recent studies indicate that HCB-induced effects in the rat may be related to autoimmunity. In Wistar rats exposed to HCB, IgM antibodies against several autoantigens were elevated; in the Lewis rat, HCB differently modulated two experimental models of autoimmune disease. Oral exposure of rats to HCB induces skin and lung pathology in the rat. Recently several studies have been conducted to investigate whether these skin and lung lesions can be related to HCB-induced immunomodulation, and these studies will be discussed in this review. HCB-induced skin and lung lesions probably have a different etiology; pronounced strain differences and correlation of skin lesions with immune parameters suggest a specific involvement of the immune system in HCB-induced skin lesions. The induction of lung lesions by HCB was thymus independent. Thymus-dependent T cells were not likely to be required for the induction of skin lesions, although T cells enhanced the rate of induction and the progression of the skin lesions. No deposition of autoantibodies was observed in nonlesional or lesional skin of HCB-treated rats. Therefore, we concluded that it is unlikely that the mechanism by which most allergic or autoimmunogenic chemicals work, i.e., by binding to macromolecules of the body and subsequent T- and B-cell activation, is involved in the HCB-induced immunopathology in the rat. Such a thymus-independent immunopathology is remarkable, as HCB strongly modulates T-cell-mediated immune parameters. This points at a very complex mechanism and possible involvement of multiple factors in the immunopathology of HCB.
PMCID: PMC1566236  PMID: 10502545
5.  Risk assessment for the harmful effects of UVB radiation on the immunological resistance to infectious diseases. 
Risk assessment comprises four steps: hazard identification, dose-response assessment, exposure assessment, and risk characterization. In this study, the effects of increased ultraviolet B(UVB, 280-315 nm) radiation on immune functions and the immunological resistance to infectious diseases in rats were analyzed according to this strategy. In a parallelogram approach, nonthreshold mathematical methods were used to estimate the risk for the human population after increased exposure to UVB radiation. These data demonstrate, using a worst-case strategy (sensitive individuals, no adaptation), that exposure for approximately 90 min (local noon) at 40 degrees N in July might lead to 50% suppression of specific T-cell mediated responses to Listeria monocytogenes in humans who were not preexposed to UVB (i.e., not adapted). Additionally, a 5% decrease in the thickness of the ozone layer might shorten this exposure time by approximately 2.5%. These data demonstrate that UVB radiation, at doses relevant to outdoor exposure, may affect the specific cellular immune response to Listeria bacteria in humans. Whether this will also lead to a lowered resistance (i.e.,increased pathogenic load) in humans is not known, although it was demonstrated that UVB-induced immunosuppression in rats was sufficient to increase the pathogenic load. Epidemiology studies are needed to validate and improve estimates for the potential effects of increased UVB exposure on infectious diseases in humans.
PMCID: PMC1533030  PMID: 9435148
6.  Contaminant-related suppression of delayed-type hypersensitivity and antibody responses in harbor seals fed herring from the Baltic Sea. 
Environmental Health Perspectives  1995;103(2):162-167.
Recent mass mortalities among several marine mammal populations have led to speculation about increased susceptibility to viral infections as a result of contaminant-induced immunosuppression. In a 2.5-year study, we fed herring from either the relatively uncontaminated Atlantic Ocean or the contaminated Baltic Sea to two groups of captive harbor seals and monitored immune function in the seals. Seals fed the contaminated fish were less able to mount a specific immunological response to ovalbumin, as measured by in vivo delayed-type hypersensitivity (DTH) reactions and antibody responses. The skin reaction to this protein antigen was characterized by the appearance of mononuclear cells which peaked at 24 hr after intradermal administration, characteristic of DTH reactions in other animals studied. These DTH responses correlated well with in vitro tests of T-lymphocyte function, implicating this cell type in the reaction. Aryl-hydrocarbon (Ah) receptor-dependent toxic equivalent (TEQ) profiles in blubber biopsies taken from the seals implicated polychlorinated biphenyls rather than dioxins or furans in the observed immunosuppression. Marine mammal populations currently inhabiting polluted coastal environments in Europe and North America may therefore have an increased susceptibility to infections, and pollution may have played a role in recent virus-induced mass mortalities.
PMCID: PMC1519003  PMID: 7737064
7.  UV-B exposure impairs resistance to infection by Trichinella spiralis. 
Environmental Health Perspectives  1994;102(3):298-301.
To assess the possibility that increases in UV-B exposure on the earth's surface could lead to impaired resistance to several infectious diseases, we studied the effect of UV-B exposure on resistance against Trichinella spiralis. Wistar rats, orally infected with T. spiralis larvae, were exposed to suberythemal doses of UV-B radiation daily for 5 days at different time periods before or after infection. A significant increase in the number of Trichinella larvae was found in the carcasses of rats irradiated with UV-B between 6 and 10 days after infection. These data indicate that exposure to UV-B radiation suppresses the resistance to a parasitic infection. We suggested that UV-B radiation especially suppresses cellular immune responses against these worms because specific IgM, IgG, and IgE titers were not significantly altered by UV-B exposure. These data indicate that UV-B irradiation plays a role in the course of infection with T. spiralis, which suggests that increases of UV-B exposure might also lead to problems with other infectious diseases and might affect vaccination because of the interaction of UV-B irradiation with memory T-cells.
PMCID: PMC1567116  PMID: 8033870

Results 1-7 (7)