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Biomedical subjects

M Friesen

Publications and source records attributed to M Friesen.

At least 19 recordsLinked to original sources
PubMed2001

Canadian guidelines for cardiac rehabilitation and atherosclerotic heart disease prevention: a summary.

Atherosclerotic heart disease (AHD) is the leading cause of death in Canadian women and men. Cardiac rehabilitation has been repeatedly shown to reduce cardiac morbidity and mortality significantly among patients with documented AHD. The Canadian Association of Cardiac Rehabilitation (CACR) has defined cardiac rehabilitation as "the enhancement and maintenance of cardiovascular health through individualized programs designed to optimize physical, psychological, social, vocational and emotional status. This process includes the facilitation and delivery of secondary prevention through heart hazard (risk factor) identification and modification in an effort to prevent disease progression and the recurrence of cardiac events". This summary presents a limited amount of background information and the majority of clinical practice recommendations contained within the previously published CACR Guidelines. These evidence-based clinical recommendations are intended as guidelines to good clinical practice rather than as standards of care. The key focus of this summary is the need for complete and targeted intervention of all heart hazards in patients at high or very high risk for, or with documented, AHD. To achieve this goal, the CACR Guidelines and this summary present risk stratification strategies designed to determine unambiguously a patient's risk of exercise-related cardiac events (short term absolute risk or disease prognosis) and their risk of recurrent AHD events (long term absolute risk from disease progression). The establishment of the short term and long term absolute AHD risks can then be used to determine heart hazard targets and the type of exercise program prescribed for patients with AHD. Despite the use of evidence-based medical practices, none of the recommendations presented in this document can replace the expert judgment of properly trained and experienced cardiac rehabilitation professionals. Health care providers must always be free to choose where and when clinical practice guidelines are applied, modified or superceded, depending on individual patient circumstances.

Canada↗
PubMed1998

Evaluation of dyspnea during physical and speech activities in patients with pulmonary diseases.

STUDY OBJECTIVES: Dyspnea is most commonly assessed by questioning patients about their subjective perception of shortness of breath during physical exertion. Although speech production is altered by pulmonary disease, it has not been included in current dyspnea assessment tools. A questionnaire was developed to address reports of dyspnea during (1) physical activity, (2) speech activity, and (3) simultaneous speech and physical activity. DESIGN: An equal number of self- and experimenter-administered 30-item questionnaires was given to 203 patients with restrictive and obstructive pulmonary diseases. Their responses were analyzed statistically. RESULTS: The questionnaire had high internal consistency for individual items within each of the three sections. The sections were highly correlated but provided separate and distinct information. Factors extracted from each section were related to severity of dyspnea. Pairwise t tests demonstrated highly significant differences in subject responses to the three sections. The least dyspnea was experienced during speech activities, more during physical activities, and the most when speech and physical activities were combined. CONCLUSIONS: The questionnaire proved to be a quickly administered tool for providing information about the effect of dyspnea on activities of daily living. Because of the emphasis on dyspnea during speech production, it may be particularly useful for assessing patients who rely extensively on speaking ability for their livelihood.

Activities of Daily Living↗
PubMed1997

In vitro activity of a new semisynthetic echinocandin, LY-303366, against systemic isolates of Candida species, Cryptococcus neoformans, Blastomyces dermatitidis, and Aspergillus species.

The in vitro activities of LY-303366, a new semisynthetic echinocandin, and comparators amphotericin B, 5-fluorocytosine, fluconazole, and ketoconazole against 205 systemic isolates of Candida species, Cryptococcus neoformans, Blastomyces dermatitidis, and Aspergillus species were determined. LY-303366 had MICs of < or = 0.32 microg/ml for all Candida albicans (n = 99), Candida glabrata (n = 18), and Candida tropicalis (n = 10) isolates tested. LY-303366 was also active against Aspergillus species (minimum effective concentration at which 90% of the isolates are inhibited, 0.02 microg/ml) (n = 20), was less active against Candida parapsilosis (MIC at which 90% of the isolates are inhibited [MIC90], 5.12 microg/ml) (n = 10), and was inactive against C. neoformans (MIC90, >10.24 microg/ml) (n = 15) and B. dermatitidis (MIC90, 16 microg/ml) (n = 29).

Anidulafungin↗
PubMed1994

Analysis of 4-aminobiphenyl-DNA adducts in human urinary bladder and lung by alkaline hydrolysis and negative ion gas chromatography-mass spectrometry.

Analysis of carcinogen-DNA adducts has been regarded as a useful means of assessing human exposure to chemical carcinogens. We have established a method for quantitation of 4-aminobiphenyl (4-ABP)-DNA adducts by alkaline hydrolysis and gas chromatography with negative ion chemical ionization mass spectrometry (GC-NICI-MS). Aliquots of DNA (typically 100 micrograms/ml) were spiked with an internal standard, d9-4-ABP, and were hydrolyzed in 0.05 N NaOH at 130 degrees C overnight. The liberated 4-ABP was extracted with hexane and derivatized using pentafluoropropionic anhydride in trimethylamine for 30 min at room temperature prior to GC-NICI-MS. With in vitro [3H]N-hydroxy-4-ABP modified DNA standards, we observed 59 +/- 7% (n = 9) recovery of the 4-ABP and a linear correlation between hydrolyzed 4-ABP and the adduct levels ranging from about 1 in 10(8) to 1 in 10(4) nucleotides (r = 0.999, n = 9). The method was further validated by comparison of the results with that obtained by the 32P-postlabeling method. There was excellent agreement (r = 0.994, p < 0.001) between the two methods for quantitation of the adduct in eight samples of Salmonella typhimurium DNA treated with 4-ABP and rat liver S9, although the 32P-postlabeling method gave slightly higher values. The DNA adducts in 11 human lung and 8 urinary bladder mucosa specimens were then determined by our GC-NICI-MS method. The adduct levels were found to be < 0.32 to 49.5 adducts per 10(8) nucleotides in the lungs and < 0.32 to 3.94 adducts per 10(8) nucleotides in the bladder samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalies↗
PubMed1993

Black (air-cured) and blond (flue-cured) tobacco cancer risk. IV: Molecular dosimetry studies implicate aromatic amines as bladder carcinogens.

Tobacco smoking causes a major fraction of male urinary bladder cancers and the relative risk of bladder cancer is reported to be two to three times higher for smoking of black (air-cured) than for smoking of blond (flue-cured) tobacco. In molecular dosimetry studies to examine the hypothesis that aromatic amines in tobacco smoke are primarily responsible for bladder cancer, the higher bladder cancer risk in smokers of black tobacco was correlated with two to five times higher exposure to carcinogenic aromatic amines present in black tobacco smoke, notably 4-aminobiphenyl (ABP). For the same amount of smoking, black tobacco smokers had levels of ABP-haemoglobin (Hb) adducts 1.5 times higher and excreted a 1.8-fold higher level of urinary mutagens. These mutagens were characterised as aromatic amines, and included the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), a known mutagen and multiorgan/species carcinogen. In smoking volunteers, the ABP-Hb adduct level depended significantly on the acetylator and P-450IA2 phenotypes, being 1.3- to 1.5-fold lower in fast acetylators, slow/intermediate P-450IA2 individuals. The N-(deoxyguanosine-8-yl)-ABP adduct was a major smoking-related DNA adduct in bladder biopsies from surgical patients. It was also tentatively identified in exfoliated urothelial cells of smoking volunteers, who showed a significant and linear correlation between adduct levels of ABP with Hb and with deoxyguanosine in urothelial DNA; both were related to number of cigarettes smoked per day. Levels of several smoking-related DNA adducts in urothelial cells were 2-20 times elevated in smokers. Similar convex dose-response relationships have been found between the number of cigarettes smoked and the relative risk for bladder cancer and between the levels of ABP-Hb adducts and markers of recent smoking. A possible explanation is that fast and slow acetylators have different susceptibility to aromatic amine carcinogens. Case-control studies have consistently revealed an excess of variable magnitude of slow acetylators in subgroups exposed occupationally to carcinogenic aromatic amines. Altogether, results from these studies reinforce the association between cigarette smoking, carcinogen-DNA adducts in urothelial cells, and implicate primary aromatic and possibly heterocyclic amines as bladder carcinogens.

Amines↗
PubMed1992

Carcinogenic tobacco-specific nitrosamines are present at unusually high levels in the saliva of oral snuff users in Sudan.

Exposure to tobacco-specific nitrosamines (TSNA) has been measured in the saliva of 12 users of Sudanese oral snuff (toombak). Using GC coupled to thermal energy analysis, levels of N'-nitrosonornicotine (NNN), N'-nitrosoanatabine (NAT), N'-nitrosoanabasine (NAB) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were measured before, during and after snuff taking. In addition, two TSNA, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and 4-(methylnitrosamino)-4-(3-pyridyl)-1-butanol (iso-NNAL), were detected in the saliva of tobacco chewers for the first time and were confirmed by GC-MS. Nine out of 10 subjects had detectable saliva levels of total TSNA before chewing (0.01-1.0 micrograms/ml) and immediately following chewing (0.1-2.6 micrograms/ml). During dipping, TSNA concentrations reached microgram/ml levels; (range; number of subjects positive) NNN: (0.6-2.1; 12/12), NAT (0.06-0.5; 2/12), NAB (0.05-1.9; 12/12), NNK (0.06-6.7; 11/12), NNAL (0.05-3.3; 11/12) and iso-NNAL (0.07-0.4; 8/12). These saliva TSNA levels, which are 10-100 times the levels previously reported, are consistent with recent observations of unusually high TSNA levels in Sudanese toombak. As several of these TSNA have been shown to be carcinogenic in animals and epidemiological studies have associated human snuff use with tumours of the oral cavity, these findings draw attention to a significant potential public health hazard.

Adolescent↗
PubMed1992

Role of lime in the generation of reactive oxygen species from betel-quid ingredients.

The role of lime in the formation of reactive oxygen species (ROS), i.e., O2-., H2O2, and OH., from betel-quid components (extracts of areca nut and catechu) was investigated in vitro using a chemiluminescence technique and an assay for oxidative DNA damage involving analysis of 8-hydroxy-2'-deoxyguanosine. Of the various areca-nut extracts, the catechin fraction, at alkaline pH, was shown to be the most active producer of ROS. The free Ca(OH)2 content and pH of lime samples (a component of betel quid and chewing tobacco) were highly correlated with the generation of ROS from areca-nut extract in vitro and with oxidative base damage to DNA in vitro. While Fe2+ had an enhancing effect on ROS formation, Mg2+ had a marked inhibitory effect. The cytogenetic effects of ROS generated in vivo were measured in Syrian golden hamsters in which the cheek pouch had been painted with lime and an areca-nut extract or catechu, singly or in combination. The frequency of micronucleated cells was increased only in animals that had received both the areca-nut extract and lime. The frequency of micronucleated cells in exfoliated oral mucosal cells from Indian chewers of betel quid with tobacco containing lime or of tobacco with lime was significantly higher than in a control (no habit) group. These studies demonstrate that addition of lime to betel quid constituents generates ROS, which induce cytogenetic damage in hamster cheek pouch and may contribute to the cytogenetic damage observed in the oral cavity of betel-quid chewers. These results implicate ROS in clastogenesis and probably in the etiology of oral cancer.

Animals↗
PubMed1991

Urinary excretion of S-benzylmercapturic acid as an indicator of N-nitroso-N-methylbenzylamine exposure.

The excretion of S-benzylmercapturic acid (SBzMA) in the urine of rats treated with N-nitroso-N-methylbenzylamine (NMBzA) was determined by gas chromatography-mass spectrometry (GC-MS). The identity of SBzMA in the urine was confirmed by full scan GC-MS. The amount of urinary SBzMA varied with the dose of NMBzA (up to 5 mg/kg) and with rat strain. For the three strains investigated, most of a 2.5 mg/kg dose of SBzMA was excreted within 24 h. Comparison of the levels of this SBzMA excreted by rats treated with equivalent doses of either NMBzA or benzaldehyde indicates that urinary SBzMA is derived mainly from benzylating species resulting from the hydroxylation of the methyl group of NMBzA.

Acetylcysteine↗
PubMed1991

32P Postlabelling analysis of urinary mutagens from smokers of black tobacco implicates 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) as a major DNA-damaging agent.

When mutagens extracted from the urine of two smokers of black tobacco were reacted with DNA in vitro in the presence of a metabolic activation system, several DNA adducts were detected by 32P-postlabelling analysis. Some of these adducts were also visible, but only faintly, on the autoradiogram for a non-smoker's urine. DNA adducts produced in vitro by 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline or 2-amino-1-methyl-6-phenylimidazo[3,5-b]pyridine could not account for the adduct pattern produced by the urinary mutagens. However, three or four 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-related DNA adducts were present among the five or six adducts observed for smokers in the autoradiograms of urinary mutagen-adducted nucleotides. Mutagenicity testing combined with HPLC fractionation of urinary extracts also supported the postlabelling data which implicates PhIP as a mutagen in the urine of smokers of black tobacco.

Chromatography, High Pressure Liquid↗
PubMed1991

Unusually high levels of carcinogenic tobacco-specific nitrosamines in Sudan snuff (toombak).

The aim of these studies was to determine the levels of carcinogenic tobacco specific nitrosamines (TSNA) in Sudanese oral snuff (toombak) as recent retrospective epidemiological studies suggested an association between the use of toombak and subsequent development of oral cancer. We have analyzed the TSNA levels in 20 samples of Sudanese toombak, of four different quality levels, collected from five different vendors. Using GC coupled with thermal energy analysis, four TSNA were quantified in snuff extracts: N'-nitrosonornicotine (NNN), N'-nitrosoanatabine (NAT), N'-nitrosoanabasine (NAB) and 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Unusually high levels of these TSNA (mean; range, mg/g snuff, dry wt) were detected; NNN (1.13; 0.50-3.08); NAT (0.08; 0.02-0.29); NAB (0.22; 0.02-2.37); and NNK (2.31; 0.62-7.87). Previously, the highest levels of NNN and NNK reported in any snuff were 0.154 and 0.014 mg/g dry wt respectively. In comparison, the levels in Sudanese toombak were up to 20 and 560 times higher respectively. As the public health implications of these findings are significant, attempts should be made to reduce exposure to TSNA in oral snuff users in Sudan.

Carcinogens↗
PubMed1991

Nitrotyrosine as a new marker for endogenous nitrosation and nitration.

A sensitive and selective method has been developed for analysing 3-nitrotyrosine (NTTYR), an exposure marker for exogenous and endogenous nitrosating or nitrating agents, in tissue and blood proteins by gas chromatography-thermal energy analysis. Using this method, a number of kinetic studies were carried out. Free and protein-bound tyrosine were reacted easily to yield NTTYR. The method was also applied to the study of NTTYR formation in vivo; a dose-dependent increase in NTTYR was seen in both plasma proteins and haemoglobin obtained from rats 24 h after intraperitoneal injection of various doses (0.5-2.5 mumol/rat) of tetranitromethane. Major urinary metabolites of NTTYR, given orally to rats, were isolated and identified as 3-nitro-4-hydroxyphenylacetic acid (NHPA) and 3-nitro-4-hydroxyphenyllactic acid. About 44% and 5% of the oral dose of NTTYR (100 micrograms/rat), respectively, was excreted as these metabolites. Some human urine samples were analysed for NHPA by gas chromatography-thermal energy analysis after ethyl acetate extraction and high-performance liquid chromatography purification; 2.8 +/- 2.3 (mean +/- SD; n = 11) micrograms/24 h, ranging from 0-7.9 micrograms/24 h, were detected (detection limit, 0.2 micrograms/l). In conclusion, NTTYR in proteins or its metabolites in urine could be readily analysed by gas chromatography-thermal energy analysis as a new, additional marker for endogenous nitrosation and nitration.

Animals↗
PubMed1990

Nitrotyrosine as a new marker for endogenous nitrosation and nitration of proteins.

3-Nitrotyrosine (NTYR) in tissue or blood proteins was evaluated as a possible exposure marker for exogenous and endogenous nitrosating or nitrating agents. A sensitive and selective method for analysing NTYR by gas chromatography with a thermal energy analyser (GC-TEA) was developed. Using this method, a number of kinetic studies were carried out. It was found that free and protein-bound tyrosine residues easily react with nitrating/nitrosating agents to yield NTYR. NTYR formation in vivo showed a dose-dependent increase in NTYR in both plasma proteins and haemoglobin obtained from rats 24 hr after ip injection of various doses (0.5-2.5 mumol/rat) of tetranitromethane. Major urinary metabolites of NTYR, given orally to rats, were isolated and identified as 3-nitro-4-hydroxyphenylacetic acid (NHPA) and 3-nitro-4-hydroxyphenyllactic acid (NHPL). About 44% and 5% of the oral dose of NTYR (100 micrograms/rat) was excreted as NHPA and NHPL, respectively. Eleven 24-hr human urine samples were analysed for NHPA by GC-TEA after ethyl acetate extraction and HPLC purification: quantities ranging from 0 to 7.9 micrograms/24 hr, mean +/- SD 2.8 +/- 2.3 (n = 11) were detected (detection limit 0.2 micrograms/litre). NTYR in proteins or its metabolites in urine can be readily analysed by GC-TEA as a new/additional marker for endogenous nitrosation and nitration.

Animals↗
PubMed1990

Effect of lime composition on the formation of reactive oxygen species from areca nut extract in vitro.

Lime, representative of that used by betel quid chewers, was collected in a region of Papua New Guinea where the incidence of oral cancer is high. The free calcium hydroxide content and pH of 25 lime samples were highly correlated with the generation of reactive oxygen species from areca nut extract in vitro, and DNA damage in vitro, measured as 8-hydroxy-2'-deoxyguanosine. Fe2+ and Mg2+ levels in the lime samples were too low to modify formation of reactive oxygen species, but hydrogen peroxide formation was almost entirely inhibited by addition of Mg2+ to the reaction mixture. These results suggest that the calcium hydroxide content of lime in the presence of areca nut is primarily responsible for the formation of reactive oxygen species which might cause oxidative damage in the DNA of buccal mucosa cells of betel quid chewers.

8-Hydroxy-2'-Deoxyguanosine↗