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Biomedical subjects

R Zamboni

Publications and source records attributed to R Zamboni.

41 records · Page 3Linked to original sources

[The assessment of exposure to the risk of the manual lifting of patients and the results of a clinical study in the rest homes of the Mantua area].

At the request of the Geriatric Residences Management Committees, the Prevention and Safety at the Workplace Service of Mantua Hospital coordinated the practical application of Chapter V of Law 626/94 with special reference to patient handling. Assessment of exposure and clinical identification of disorders and impairment of the lumbar spine carried out using the methods proposed by the EPM Research Centre involved 15 residences and a total of 31 departments analyzed and 435 workers submitted to health surveillance by the respective certified occupational physicians. With the exception of one department, the exposure levels were found to be medium-high (MAPO Index > 1.51) considering the number of disabled patients, the significant lack of lifting equipment and the lack of training for this risk factor. Acute low back pain reported in the previous 12 months revealed a prevalence of 10%, more than 4 times that of non-exposed workers. The prevalence of functional spondylarthropathies also showed high values (16%), as also the number of degenerative diseases of the lumbosacral spine (16%). 11% of the males and 17% of the females were judged unfit for patient handling, which created problems of job reallocation. By concentrating the results at the Prevention and Safety at the Workplace Service it was possible to plan interventions for improvement, using as referents for the various residences a working group where the presence of a qualified physiotherapist proved to be particularly useful. Coordination of the certified occupational physicians also improved the quality of health surveillance.

Adolescent↗

In vitro and in vivo biotransformations of the potent leukotriene D4 antagonist verlukast in the rat.

Verlukast, (S)3-((((3-(2-(7-chloroquinolin-2-yl)-(E)-ethenyl)phenyl)- 3-dimethylamino-3-oxopropylthio)methyl)thio)propionic acid, formerly known as MK-679, is a potent leukotriene D4 antagonist. Verlukast was incubated with rat liver microsomes under oxidative conditions to generate five metabolites, which were identified as the four possible isomeric monosulfoxides (M1-M4), and the N-hydroxymethyl amide (M5). This latter metabolite loses the elements of formaldehyde to yield the N-monomethyl amide (M6). These metabolites were isolated from a large microsomal incubation and were characterized by UV, 1H-NMR, and fast atom bombardment-MS. These data were identical to those obtained from synthetically prepared standards. Microsomal incubations of verlukast supplemented with UDP-glucuronic acid yielded the acyl glucuronide metabolite (M7), which was isolated and characterized by UV, 1H-NMR, and fast atom bombardment-M5. Verlukast was regenerated from M7 upon treatment with either beta-glucuronidase or strong aqueous base (pH greater than 11). The metabolites described above were all detected in bile collected from a rat dosed with verlukast.

Animals↗

Characterization of verlukast metabolites arising from an epoxide intermediate produced with hepatic microsomes from beta-naphthoflavone-treated rodents (P-4501A1).

Verlukast, (R)3-((((3-(2-(7-chloroquinolin-2-yl)-(E)-ethenyl)phenyl)-3- dimethylamino-3-oxopropylthio)methyl)thio)-propionic acid (also known as MK-0679 and L-668,019), is a potent leukotriene D4 antagonist. Verlukast was incubated with hepatic microsomes from beta-naphthoflavone (beta NF) or isosafrole-treated rodents to evaluate whether P-4501A1 or 1A2 mediated biotransformations could occur. With beta NF-induced mouse or rat microsomes, in which the induction of P-4501A1 had been proven by Western blot analysis, incubations produced new metabolites that were separated by reversed-phase HPLC and were initially characterized by UV (photodiode array). Metabolites were subsequently isolated and characterized by NMR and MS, and were assigned as the 5",6"-dihydrodiol and 6"-phenol (on the quinoline ring). The presumed 5",6"-epoxide intermediate was also detected and was characterized by UV (photodiode array) and MS. Microsomes from isosafrole-treated rodents produced the dihydrodiol to a much lesser extent and did not yield any other new metabolites. alpha-Naphthoflavone inhibited the dihydrodiol formation in incubations with microsomes from isosafrole- and beta NF-treated rats. In incubations with microsomes from beta NF-treated rats, to which the epoxide hydrolase inhibitor 3,3,3-trichloropropene 1,2-oxide had been added, the formation of dihydrodiol was inhibited, consistent with a microsomal epoxide hydrolase hydrolysis of the epoxide intermediate. When glutathione was added to incubations with microsomes from beta NF-treated rats, the dihydrodiol, phenol, and epoxide peaks were reduced in size and a new material, the glutathione adduct, was formed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗