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Bacterial flora

The main difficulty in preparing a sediment reference material for interlaboratory studies on chemical species is to achieve the stability of the relevant compounds [12]. With respect to methylmercury, the main source of instability is due to bacteria, either by demethylation [88,89] or formation of volatile dimethylmercury [90]. The conversion is indirectly provoked by the biological activity of various types of bacteria, such as (i) aerobic mesophilic heterotrophic microorganisms, (ii) anaerobic sulfate-reducing bacteria and (iii) anaerobic spore-forming bacteria. In order to control the remaining bacteria present after different irradiation treatments, a bacterial enumeration was performed on samples which were dehydrated after homogenization and irradiated at various 7-ray doses (0, 4, 8, 12, 25 and 50 kGy). The determination of the sulfate- [Pg.61]

The cultivable bacteria of the three groups were high in sediment samples analysed immediately after drying and homogenization processes (non-irra-diated samples). In the sample irradiated at the 4 kGy dose, the bacteria content was significant for the heterotrophic and the spore-forming bacterial group, whereas the sulfate reducers were inhibited. [Pg.62]

As a conclusion of these tests, the y-irradiation of sediment at 8 kGy was found to be able to sterilize the sediment completely. [Pg.62]


Cobalt is one of twenty-seven known elements essential to humans (28) (see Mineral NUTRIENTS). It is an integral part of the cyanocobalamin [68-19-9] molecule, ie, vitamin B 2> only documented biochemically active cobalt component in humans (29,30) (see Vitamins, VITAMIN Vitamin B 2 is not synthesized by animals or higher plants, rather the primary source is bacterial flora in the digestive system of sheep and cattle (8). Except for humans, nonmminants do not appear to requite cobalt. Humans have between 2 and 5 mg of vitamin B22, and deficiency results in the development of pernicious anemia. The wasting disease in sheep and cattle is known as bush sickness in New Zealand, salt sickness in Florida, pine sickness in Scotland, and coast disease in AustraUa. These are essentially the same symptomatically, and are caused by cobalt deficiency. Symptoms include initial lack of appetite followed by scaliness of skin, lack of coordination, loss of flesh, pale mucous membranes, and retarded growth. The total laboratory synthesis of vitamin B 2 was completed in 65—70 steps over a period of eleven years (31). The complex stmcture was reported by Dorothy Crowfoot-Hodgkin in 1961 (32) for which she was awarded a Nobel prize in 1964. [Pg.379]

In all antiseptic testing, it is recognized that skin and mucous membranes to which products ate appHed cannot be disinfected or sterilized but it is possible to significantly reduce the population of transient and resident pathogenic bacterial flora. AH in vivo test methods requite a deterrnination of the bacteria on the skin before and after treatment. Because of the normal variation in bacterial population of the skin of different people, a number of people must be tested in order to make a statistical analysis of the results. Different parts of the body are used for different tests. In aH of the tests the details of the protocol ate extremely important and must be strictly adhered to in order to obtain reproducible results. [Pg.140]

The body possesses a normal bacterial flora which, by competing for essential nutrients or by the production of inhibitoiy substances such as monolactams or colicins, suppresses the growth of many potential pathogens. [Pg.280]

Styrene-degrading bacteria from full-scale and experimental biofilters were exposed to [ HJstyrene, and analysis of fatty acids was used to distinguish the bacterial flora of the two systems (Alexandrino et al. 2001). [Pg.279]

Antibiotics have been studied based on the rationale that they may interrupt the inflammatory response directed against endogenous bacterial flora. Metronidazole and ciprofloxacin have been the two most widely-studied agents.32 Metronidazole may benefit some patients with pouchitis (inflammation of surgically-created intestinal pouches) and patients with CD who have had ileal resection or have perianal fistulas. Ciprofloxacin has shown some efficacy in refractory active CD. Both drugs may cause diarrhea, and long-term use of metronidazole is associated with the development of peripheral neuropathy. [Pg.288]

Local host defenses of both the upper and lower respiratory tract, along with the anatomy of the airways, are important in preventing infection. Upper respiratory defenses include the mucodliary apparatus of the nasopharynx, nasal hair, normal bacterial flora, IgA antibodies, and complement. Local host defenses of the lower respiratory tract include cough, mucodliary apparatus of the trachea and bronchi, antibodies (IgA, IgM, and IgG), complement, and alveolar macrophages. Mucus lines the cells of the respiratory tract, forming a protective barrier for the cells. This minimizes the ability of organisms to attach to the cells and initiate the infectious process. The squamous epithelial cells of the upper respiratory tract are not ciliated, but those of the columnar epithelium of the lower tract are. The cilia beat in a uniform fashion upward, moving particles up and out of the lower respiratory tract. [Pg.1050]

Colonization and metabolic activity of gastrointestinal bacterial flora do not approach adult values until 2-4 years of age [19]. This has resulted in increased bioavailability of digoxin in infants and young children. [Pg.668]

In contrast to segmentation contractions in the small intestine (9 to 12 per minute), haustral contractions occur much less frequently (up to 30 min between contractions). These very slow movements allow for the growth of bacteria in the large intestine. Normally, the bacterial flora in this region is harmless. In fact, some of the bacteria produce absorbable vitamins, especially vitamin K. [Pg.304]

It is thought that bicarbonate excretions by oral tissues and the neutral pH of the saliva maintain a neutral pH in the areas inhabited by nitrite-producing bacteria, thus preventing nitrite becoming toxic to the resident bacterial flora in the oral cavity. As with denitrifying bacteria isolated from other environments... [Pg.255]

Drasar BS, Shiner M, Mcloed GM Studies on the intestinal flora. The bacterial flora of the gastrointestinal tract in healthy and achlorhydric persons. Gastroenterology 1969 56 71— 79. [Pg.18]

Ruddel WWJ, Axon ATR, Findlay JM, Bartholomew BA, Hill MJ Effect of cimetidine on the gastric bacterial flora. Lancet 1980 i 672-674. [Pg.19]

Johanson WG, Pierce AK, Sanford JP Changing pharyngeal bacterial flora of hospitalized patients. N Engl J Med 1969 281 1137-1140. [Pg.19]

Greenlee HB, Vivit R, Paez J, Dietz A Bacterial flora of the jejunum following peptic ulcer surgery. Arch Surg 1971 102 260-265. [Pg.19]

Bishop RF, Andersson CM The bacterial flora of the stomach and small intestine in children with intestinal obstruction. Arch Dis Child 1960 35 487 191. [Pg.20]

Toskes PP, Donaldson RM Enteric bacterial flora and bacterial overgrowth syndrome in Sleisenger MH, Fordtran JS (eds) Gastrointestinal Disease. Philadelphia, Saunders, 1993, pp 1106-1125. [Pg.20]

Tabaqchali S The pathophysiological role of small intestinal bacterial flora. Scand J Gastroenterol Suppl 1970 6 139-163. [Pg.21]

Animal studies indicate that the pathogenesis of NSAID small intestinal toxicity involves multiple interactions dependent on enterohepatic circulation, epithelial permeability, neutrophil infiltration and bacterial infection [233]. Several investigations [234-238] have suggested that bacterial flora may play a role in the pathogenesis of NSAID bowel injury and Robert and Asano [239] did show more than 25 years ago that germ-free rats are resis-... [Pg.56]

Linskens RK, Huijsdens XW, Savelkoul PH, Vandenbroucke-Grauls CM, Meuwissen SG The bacterial flora in inflammatory bowel disease Current insights in pathogenesis and the influence of antibiotics and probiotics. Scand J Gastroenterol 2001 36(suppl 234) 29-40. [Pg.66]

In a recent study, we found no acquisition of rifaximin resistance in 27 rifaximin-treated subjects colonized by Enterococcus [37]. The MIC50 and MIC90 for the treatment group (rifaximin at a dose of either 400 or 200 mg twice daily for 3 days) were similar (16-64 pg/ml). In two published studies, rifaximin resistance was shown to occur in the bacterial flora of individuals who received treatment with rifaximin at a dose of 800 mg/day for 5 days [9, 27]. Within 1-2 weeks after the end of rifaximin treatment, resistance rates appeared to have decreased to less than 20% of the intestinal flora. The resistant strains detected during treatment appeared to be unstable and unable to persistently colonize the intestinal tract. [Pg.71]

Table 3. Antibiotic effect on suppression of normal bacterial flora of humans... [Pg.84]

Hill MJ, Drasar BS The normal colonic bacterial flora. Gut 1975 16 318—323. [Pg.88]

Vergnes D, Moatti N, Monrozies X, Lazorthes F, Enjalbert L Pre-operative colonic preparation using kanamycin and metronidazole Qualitative and quantitative effects on the bacterial flora of the intestine. J Antimicrob Che-mother 1980 6 709-716. [Pg.88]

Welling GW, Meijer-Severs GJ, Helmus G, van Santen E, Tonk RH, de Vries-Hospers HG, van der Waaij D The effect of ceftriaxone on the anaerobic bacterial flora and the bacterial enzymatic activity in the intestinal tract. Infection 1991 19 313-316. [Pg.89]

Ammonia Bacterial flora Benzodiazepines, endogenous Encephalopathy, hepatic Liver cirrhosis Rifaximin... [Pg.90]

In order to ascertain whether bacterial flora is implicated in the synthesis of these compounds, we measured serum NBZD levels in patients with liver cirrhosis before... [Pg.92]

Finally, suppression of the contaminating bacterial flora represents the major aim of treatment for SIBO. [Pg.104]

Sherwood WC, Goldstein F, Haurani FI, et al Studies of the small intestinal bacterial flora and of intestinal absorption in pernicious anemia. Am J Dig Dis 1964 9 416-425. [Pg.108]

Goldstein F, Wirts CW, Kramer S The relationship of afferent loop stasis and bacterial flora to the production of postgastrectomy steatorrhea. Gastroenterology 1961 40 47-54. [Pg.108]


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See also in sourсe #XX -- [ Pg.90 ]




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