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Toxins exposure

Usually, it takes years of toxin exposure to cause the pathological alterations seen in COPD. In most cases, the disease is already well-progressed when COPD is diagnosed. Reversal of established chronic inflammatory disease is always extremely difficult to achieve and at present healing of COPD is impossible. Smoking cessation is the single most effective and cost-effective... [Pg.364]

The observed toxicity seems to depend strongly on the form of toxin exposure. In contrast to the findings obtained with dissolved toxins, no feeding responses or toxicity in copepods were observed when the diatom-toxin domoic... [Pg.189]

Carmichael WW, Azevedo SFMO, An JS, Molica RJR, Jochimsen EM, Lau S, Rinehart KL, Shaw GR, Eaglesham GK (2001) Human fatalities from cyanobacteria chemical and biological evidence for cyanotoxins. Environ Health Persp 109 663-668 Codd GA, Bell SG, Kaya K, Ward CJ, Beattie KA, Metcalf JS (1999) Cyanobacterial toxins, exposure routes and human health. Eur J Phycol 34 405 115 Cronin G, Hay M (1996) Induction of seaweed chemical defenses by amphipod grazing. Ecology 77 2287-2301... [Pg.116]

Prominent symptoms of anxiety that are judged to be a direct physiological consequence of a drug of abuse, a medication or toxin exposure... [Pg.408]

Performance of Schemes Based upon Tolerance Sets and Limiting Distributions for Evaluating Acute Exposures to Lethal Toxins. [Exposure Limit = 10.0]... [Pg.450]

Codd GA, Bell SG, Kaya K, Ward CJ, Beattie KA, Metcalf JS (1999) Cyanobacterial Toxins, Exposure Routes and Human Health. Eur J Phycol 34 405... [Pg.506]

Joseph, A.M., S.S. Hecht, S.E. Murphy, S.G. Carmella, C.T. Le, Y. Zhang, S. Han, and D.K. Hatsukami. 2005. Relationship between cigarette consumption and biomarkers of tobacco toxin exposure. Cancer Epidemiol. Biomarkers Prev. 14(12) 2963-2968. [Pg.50]

Boyd JA, Clark GC, Walmer DK, et al. 1995. Endometriosis and the environment biomarkers of toxin exposure. Abstract of Endometriosis 2000 Workshop, May 15-17. [Pg.592]

Alveoli represent the primary site for gas exchange within the lung, and thus their health is vital for survival. Alveolar conditions with a primary genetic cause, such as surfactant protein-B (SP-B) deficiency and SP-C deficiency, are prime candidates for a rAAV-gene therapy approach. Diseases in which alveoli are damaged secondary to other defects might also be treated with gene transfer. Such conditions include environmental toxin exposure, infectious diseases, and adult respiratory distress syndrome (ARDS) (Table 4.1) (Rolls et al., 1997, 1998, 2001 Cheers et al 1999 Ruan et al., 2002). [Pg.85]

For the investigation of expression changes due to xenobiotic/toxin exposure, proteins have to be extracted from samples of body fluids, tissues or cells. For this purpose, many protein extraction protocols have been developed and adapted to different sample types (Link 1999). All protocols follow the main objective to recover as much of the proteome as possible with as little contamination by other biomaterials as possible. Sample preparation has to be performed prior to any proteomics technology used in investigative studies, or predictive toxicology. Depending on the method used for protein expression analysis, fractionation steps have to follow or have to be implemented in the extraction procedures (Wilkins et al. 1997 Rabilloud 2000 Liebler 2002). [Pg.859]

After xenobiotic/toxin exposure, differentially expressed proteins are identified by the comparison of SELDI spectra from control and treated samples. By combining groupwise statistics with N-fold regulations, single biomarkers (m/z) can be selected. As to be expected from the complexity of the proteome, in many cases no single marker will be able to discriminate between the groups. Rather, a complex pattern of multiple markers will be acquired (Figure 8). Discovery of such markers/pattems can be successful by application of multivariate statistics methods on the data set. However, for the identification of specific protein expression patterns bioinformatics tools are... [Pg.867]

Apoptotic cells in any system can die and disappear relatively quickly. The time from initiation of apoptosis to completion can occur as quickly as 2-3 hr. Therefore a false negative can occur if the assay is done too early or too late. Moreover, apoptosis can occur at low frequency or in specific sites within organs, tissues, and cultures. In such cases, the ability to rapidly survey large areas could be useful. In general, if detailed information on the mechanism of cell death is desired, the duration of toxin exposure, the concentration of the test compound, and the choice of assay endpoint become critical. [Pg.313]

One essentially unexplored area for hair analysis is its application to the investigation of environmental toxin exposure. We received a research grant during 1979 from the National Institute of Occupational Safety and Health to explore the possibility of using hair analysis for monitoring exposure to polychlorinated biphenyl compounds (PCBs). Although the analytical chemical problems of this project were successfully solved, we were unable to mount successful field studies with human subjects. [Pg.261]

Hydrogen sulfide can also affect the eyes of an individual exposed to this toxin. Exposure to only 20 to 50 ppm for one hour may cause damage to the eye. Thus exposure to the eyes is to be avoided. [Pg.248]

The exposure to lead based paints and subsequent lead nephropathy and encephalopathy, in the USA, is concentrated in substandard housing [162]. Individuals at the lower end of our economic ladder often are denied access to preventative health care thus putting them at additional risk for toxin exposure. Another example is the consumption of "moonshine" whiskey that has been associated with the development of lead nephropathy [167]. [Pg.18]

Since toxin induced chronic renal failure is theorized to occur after years of low-level toxin exposure, it stands to reason that the incidence would be clustered in elderly patients. The study of Chester et al. [172] provides indirect support that elderly patients may be at greater risk. Of the 79 patients with chronic renal failure who met age criteria of 70 year or more, 29% were classified as having chronic interstitial nephritis, a clinical diagnosis quite compatible with toxin induced renal failure and an incidence substantially higher than the 10.4% in accumulated series in which patients 50 year and older were included [173]. Furthermore, in the 2006 USRDS survey of causes of ESRD, the average age for patients with a diagnosis of interstitial nephropathy was 56 year compared to 58 years for the entire population reported [119]. In the recent analysis of the PICARD database, advanced age was associated with increased mortahty in AKI patients both at time of consultation and after initiation of dialysis treatment [38]. [Pg.19]

L chain or Di-chain-toxin If the biological poisoning pathway is being used, the toxins must be in their di-chain form. Isolated L chains cannot enter the cell and are thus ineffective when added to intact cells or isolated nerve terminals. However, isolated L chains block exocytosis if they are introduced directly into the cytoplasm, e.g., by microinjection (Penner ef al., 1986 Mochida ef al., 1989 Hunt ef al., 1994), by permeabilization of the cells prior to toxin exposure (Bittner and Holz, 1988 Ahnert-Hilger efal., 1989a,b, and this volume. Chapter 18 Dayanithi ef al., 1992), or by expression of recombinant L chains (Mochida efal., 1990, Sweeney efal., 1995). These techniques allow the inhibition of exocytosis in neurosecretory cells that are toxin-resistant due to a lack of receptors. Likewise, only the free L chains (reduced di-chain toxin or isolated L chain) are active towards the respective substrates in vifro (Schiavo ef al., 1992 Link ef al., 1992 Schiavo efal., 1993c Link efal., 1994). [Pg.195]

Chronic algal toxin exposure remains mostly unstudied, although some limited information about specific toxins is included in the descriptions that follow. On the other hand, exactly how some of these toxins affect cells and tissues (mechanism of action) has received considerable attention from researchers. [Pg.69]

Poisoning may occur through ingestion, drinking tea, or smoking the plant. Seeds have the highest concentration of toxin. Exposure may be unintentional or for experimentation purposes due to the hallucinogenic properties of the plant. [Pg.2029]

Surprisingly little research has been performed on the otic effects of chemicals on workers. However, several widely used chemicals are known to be ototoxic. However, the combination of toxin exposure and noise may be additive or synergistic in the production of hearing loss. This has made investigation of the isolated toxic effects on exposed workers difficult (Table 3). [Pg.2367]

Response of living cells or tissue to pathogen or toxin exposure,... [Pg.82]

Chlorella improves blood oxygenation, digestion, and waste elimination. In addition, research has shown that it binds to and escorts toxins and heavy metals such as mercury (the dangerous metal used in many old dental amalgams) out of the body.2 Regardless of whether you re drinking green drinks, I recommend chlorella. Even the healthiest people will benefit from one of nature s richest superfoods, but it s particularly beneficial for those who suspect mercury toxicity or another type of environmental toxin exposure. [Pg.109]

An initial evaluation of male infertility should include a detailed history and physical examination with special emphasis on the reproductive organs for evidence of proper androgenization. The history must include prescribed medications, recreational and performance-enhancing drug and alcohol use, systemic illnesses, and potential toxin exposure. A sexual history should include sexual technique and frequency of intercourse. Issues of potency must be distinguished from those of infertility or subfertiHty. [Pg.2121]


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See also in sourсe #XX -- [ Pg.463 ]




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