Musculoskeletal disorders and functional characteristics of the neck and shoulder: Comparison between office workers using a laptop or desktop computer.

Background: Using a laptop for work is gaining rapid popularity, but there is little evidence of how it influences musculoskeletal disorders (MSDs) and functional characteristics of the neck and shoulder area.

Objective: This study aimed to compare the prevalence of upper body MSDs and functional characteristics of the neck between office workers using a laptop or desktop computer.

Methods: A total of 110 office workers with a mean age of 41±10 years participated.

Musculoskeletal disorders and associated factors among office workers in an activity-based work environment.

This study aimed to evaluate the prevalence of musculoskeletal disorders (MSDs) and associated factors among office workers working in the activity-based workplace (ABW). Forty-two office workers with an ABW and 68 office workers as controls participated. The Nordic musculoskeletal questionnaire, the Baecke physical activity questionnaire, the Copenhagen psychosocial questionnaire III and the fear-avoidance beliefs questionnaire were used and the pain pressure threshold (PPT) was measured.

Effects of the COVID-19 lockdown on musculoskeletal pain, physical activity, and work environment in Estonian office workers transitioning to working from home.

Background: COVID-19 lockdown caused a sudden change in the work culture and environment.

Objective: The aim of this study was to evaluate the impact of COVID-19 lockdown caused changes in musculoskeletal pain (MSP), physical activity (PA), workplace properties, and their in-between relationships among office workers.

Methods: A total of 161 office workers (64.

Development of structure-activity relationship rules for predicting carcinogenic potential of chemicals.

Since the inception of Section 5 (Premanufacturing/Premarketing Notification, PMN) of the Toxic Substances Control Act (TSCA), structure-activity relationship (SAR) analysis has been effectively used by U.S. Environmental Protection Agency's (EPA) Structure Activity Team (SAT) in the assessment of potential carcinogenic hazard of new chemicals for which test data are not available.

Assessment of carcinogenic hazard of chemical mixtures through analysis of binary chemical interaction data.

Assessment of the potential health hazard of environmental complex chemical mixtures is one of the most difficult and challenging problems in toxicology. In this article, we describe the development of an innovative computerized system for ranking and predicting potential cancer hazard of chemical mixtures. We take into consideration both the additive risk of individual carcinogens present and the projected overall interaction effect of the mixture based on analyzing and integrating the possible interaction effects of all binary pairs of individual constituents of the mixture.

Chemical carcinogens. A review and analysis of the literature of selected chemicals and the establishment of the Gene-Tox Carcinogen Data Base. A report of the U.S. Environmental Protection Agency Gene-Tox Program.

The literature on 506 selected chemicals has been evaluated for evidence that these chemicals induce tumors in experimental animals and this assessment comprises the Gene-Tox Carcinogen Data Base. Three major sources of information were used to create this evaluated data base: all 185 chemicals determined by the International Agency for Research on Cancer to have Sufficient evidence of carcinogenic activity in experimental animals, 28 selected chemicals bioassayed for carcinogenic activity by the National Toxicology Program/National Cancer Institute and found to induce tumors in mice and rats, and 293 selected chemicals which had been evaluated in genetic toxicology and related bioassays as determined from previous Gene-Tox reports. The literature data on the 239 chemicals were analyzed by the Gene-Tox Carcinogenesis Panel in an organized, rational and consistent manner.

Comparative pulmonary tumorigenesis in DBA/2J and C57Bl/6J mice by administration of 3-methylcholanthrene and dimethylnitrosamine singly and combined.

C57Bl/6J mice, which are inducible for both hepatic and pulmonary aryl hydrocarbon hydroxylase (AHH), and DBA/2J mice, which are noninducible for hepatic AHH but moderately inducible for pulmonary AHH, received dimethylnitrosamine (DMN) i. p., or methylcholanthrene (MCA) orally, or a combination of both agents, for 10 weeks; the animals were observed for an additional 26 weeks.

Interaction of the tobacco-specific nitrosamines, methylethylnitrosamine and N-nitrosonornicotine, with DNA and guanosine.

In vitro binding of the tobacco-specific nitrosamines, methylethylnitrosamine (MEN) and nitrosonornicotine (NNN), to exogenous DNA and guanosine was studies in a rat liver microsome-catalyzed system. MEN (N-[ethyl-1-14C]) binds covalently to calf thymus DNA whereas NNN (N'-[pyrrolidine-2-14C]) binds only to guanosine but not to DNA. Pretreatment of the rats with either phenobarbital (PB) or 3-methylcholanthrene (MC) greatly diminishes the binding of 14C-MEN to DNA.

Comparative effects of indole and aminoacetonitrile derivatives on dimethylnitrosamine-demethylase and aryl hydrocarbon hydroxylase activities.

The effect of in vivo administration of indole and five 3-indolyl derivatives including L-tryptophan, as well as of aminoacetonitrile and 3 of its derivatives, were studied on the carcinogen-metabolizing hepatic mixed-function oxidases dimethylnitrosamine (DMN)-demethylase I and II and aryl hydrocarbon hydroxylase (AHH). Indole, 3-indolylmethanol, 3-indolyl-acetonitrile, 3-indolylacetone and L-tryptophan induce AHH activity from 3- to 6-fold of the control level, whereas beta-3-indolylethanol has no effect; the latter compound produces a 21% decrease of the endoplasmic reticulum content in the tissue. Only L-tryptophan induces DMN-demethylase I and only L-tryptophan and 3-indolylmethanol induce DMN-demethylase II, representing a doubling of enzyme activity in all 3 instances.

Enhancement of toxicity and enzyme-repressing activity of p-dioxane by chlorination: stereoselective effects.

The acute toxicity of p-dioxane may be enhanced up to 1000-fold by chlorination of the compound. The effect was stereoselective. Of the stereoisomers tested, tetrachloro-p-dioxane, isomer I (2r, 3t, 5t, 6c) was over 80 times more toxic than isomer II (2r, 3c, 5t, 6t).

Role of dimethylnitrosamine-demethylase in the metabolic activation of dimethylinitrosamine.

In vivo administration to rats of the mixed-function oxidase modifiers 3-methylcholanthrene (MC), pregnenolone-16 alpha-carbonitrile (PCN) or beta-naphthoflavnoe (beta-f) inhibits the hepatic microsome-catalyzed in vitro binding of dimethylnitrosamine (DMN) to DNA. This parallels their effect on DMN-demethylase I, regarded to be the sole activating step in DMN carcinogenesis and fails to account for the previously observed anomaly that MC and PCN inhibit, while beta-NF enhances, the hepatocarcinogenic activity of DMN. The in vitro binding of DMN is clearly dependent on microsomes and NADPH, and is strongly enhanced by soluble cytoplasmic proteins; the presence of the latter has no effect.

Differential effects of beta-naphthoflavone and pregnenolone-16alpha-carbonitrile on dimethylnitrosamine-induced hepatocarcinogenesis.

The effect of administration of beta-naphthoflavone (beta-NF) or pregnenolone-16alpha-carbonitrile (PCN) on the hepatocarcinogenicity of dimethylnitrosamine (DMN) in male SD rats was explored. Both beta-NF and PCN are potent repressors of the low Michaelis constant enzymatic form of DMN-demethylase, a mixed-function oxidase that catalyzes DMN demethylation. DMN-induced hepatocarcinogenesis was inhibited by PCN and was enhanced by beta-NF.

Ultrastructural and metabolic determinants of resistance to azo-dye susceptibility to nitrosamine carcinogenesis of the guinea-pig.

During diethylnitrosamine (DEN) administration, a distinctive difference was observed between rats and guinea-pigs in the sequence of ultrastructural changes in the hepatic endoplasmic reticulum (ER). In DEN-induced hepatic tumour cells in the guinea-pig there was extensive proliferation of the rough ER, while the smooth ER was quite sparse; in the premalignant liver the opposite was noted. This is in contrast to the rat, in which administration of either DEN or 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) brings about, in both premalignant and malignant hepatic tissue, proliferation of the smooth ER and sparsity of the rough ER.

Structural identification of p-dioxane-2-one as the major urinary metabolite of p-dioxane.

Analysis by gas chromatography (GC) of the volatile compounds present in the urine from rats administered dioxane, a hepatic carcinogen to this species, revealed a major metabolite. The appearance of the metabolite was pH-dependent, undetectable at high pH; reacidification of the urine sample brought about the reappearance of the metabolite. The amount excreted was dose-dependent and time-dependent, reaching a maximum between 20 and 28 h after dioxane administration.

Mitochondrial membrane-linked reactions in carcinogenesis: change in steroselective uncoupling of oxidative phosphorylation by aliphatic dicarbonyls and in the Arrhenius plot of NADH-indophenol reductase.

The previously observed alterations in the energy transducing system of rat liver mitochondria during 3'-methyl-4-(dimethylamino)azobenzene (3'-Me-DAB) carcinogenesis were investigated using aliphatic dicarbonyl compounds as molecular probes and the effect of temperature on the membrane-linked NADH-indophenol reductase. The vicinal diketone, diacetyl, uncouples oxidative phosphorylation in normal rat liver mitochondria while the higher diketones, acetylacetone and acetonylacetone, are increasingly less effective in that order; diacetyl totally abolishes respiratory control with substrates the oxidation of which involves the NADH leads to CoQ segment, but only partially with succinate which bypasses this segment. Diacetyl, likewise, uncouples oxidative phosphorylation in liver mitochondria from rats fed 3'-Me-DAB, but the mitochondria are most resistant to this uncoupling (in terms of the P/O ratio) at the time period when the respiratory control index (determined in the absence of diacetyl) is at the dye-induced minmum.