Analysis of Endodontist Posture Utilizing Cinemetry, Surface Electromyography and Ergonomic Checklists

The postural risk factors for dentists include the ease of vision in the workplace, cold, vibration and mechanical pressure in tissues, incorrect posture, functional fixity, cognitive requirements and work-related organizational and psychosocial factors. The objective was to analyze the posture of endodontists at the workplace. Eighteen right-handed endodontists aged 25 to 60 years (34±3) participated in the study. Electromyography, kinemetry, ergonomic scales (RULA and Couto's checklist) and biophotogrammetry were used to analyze the posture of endodontists during root canal treatment of the maxillary right first and second molars using rotary and manual instrumentation. The variations observed in the electromyographic activities during the performance of rotary and manual techniques suggest that the fibers of the longissimus region, anterior and medium deltoid, medium trapezium, biceps, triceps brachii, brachioradialis and short thumb abductor muscles underwent adaptations to provide more accurate functional movements. Computerized kinemetry and biophotogrammetry showed that, as far as posture is concerned, rotary technique was more demanding than the manual technique. In conclusion, the group of endodontists evaluated in this study exhibited posture disorders regardless of whether the rotary or manual technique was used.

Os fatores de risco posturais para cirurgiões dentistas incluem o acesso a visão no local de trabalho, frio, vibração, pressão mecânica nos tecidos, postura incorreta, alterações funcionais, requisitos cognitivos e fatores organizacionais e psicossociais relacionados com o trabalho. O objetivo é analisar a postura dos endodontistas no local de trabalho. Participaram dezoito endodontistas destros com idades entre as idades de 25 e 60 anos (34±3). Nesta pesquisa foi utilizado a eletromiografia, cinemetria, escalas de ergonomia (do RULA e Couto checklist) e biofotogrametria para analisar a postura dos endodontistas durante o preparo químico-mecânico do sistema de canais radiculares para primeiros e segundos molares superiores direitos, utilizando a instrumentação rotatória e manual. As variações observadas nas atividades eletromiográficas durante a execução das técnicas rotatórias e manuais sugerem que as fibras da região dos músculos longuíssimo, deltóide anterior e médio, trapézio médio, bíceps, tríceps braquial, braquiorradial e músculos abdutores curtos do polegar passaram por adaptações para promover movimentos funcionais mais precisos. A cinemetria e biofotogrametria computadorizada mostraram que a técnica rotatória foi mais exigente da postura corporal do que a técnica manual. Em conclusão, os endodontistas estudados apresentaram distúrbios de postura, independentemente da técnica utilizada, rotatória ou manual.

Dietary supplementation of vitamin A, C and E prevents p-dimethylaminoazobenzene induced hepatic DNA damage in rats.

The preventive effect of antioxidant vitamins A, C, E and their analogues against DNA damage induced by a hepatocarcinogen p-dimethylaminoazobenzene (DAB) was assessed by comet assay. For genotoxicity (DNA damage) study, male albino rats were divided into 11 groups, consisting of four rats each. Group I served as control. Group II to VII received 1, 10, 100, 200, 300 and 400 mg per kg body wt of DAB respectively; group VIII to XI received 500 mg/kg body wt of DAB. They were sacrificed by cervical decapitation 3, 6, 12 and 24 h after treatment; livers were excised immediately and subjected to comet assay to measure DNA damage. To study the effect of vitamins, experiments were conducted on a group of 275 rats divided into 3 sets of 25 rats each. First set served as control; second set received 0.06% DAB and third set received 0.06% DAB, along with analogues of vitamins A, C and E. Rats fed with 0.06% DAB were provided water ad libitum for a period of 4 months, followed by a normal (basal) diet for further 2 months. Vitamins A (10,000-50,000 IU), C (75-1000 mg) and E (50-500 mg) and their analogues were given (per kg body wt) to the third set of rats by gavage route once in a week for a period of 6 months. The DAB induced DNA damage only at the highest tested dose of 500 mg/kg body wt. Administration of high doses of vitamin A acid, L-ascorbic acid and vit. E succinate individually prevented the DNA damage. However, administration of a mixture of these vitamins at low doses prevented the DAB-induced DNA damage, which may be due to their synergistic effect. The results indicate that there is a significant advantage in mixed vitamins therapy at low dose over the treatment with individual vitamins.

Protective action of an anti-oxidant (L-Ascorbic acid) against genotoxicity and cytotoxicity in mice during p-DAB-induced hepatocarcinogenesis.

BACKGROUND: DNA damage from micronutrient deficiencies has been suggested as one major cause of cancer. Therefore studies involving vitamin supplementation, particularly with those with anti-oxidant activity, in combating cancer have routinely been carried out in both in vivo and in vitro systems, but relatively much less in mice. AIMS: The present study examines if L-Ascorbic acid (AA; vitamin C) administration has any protective abilities in combating p-DAB induced hepatocarcinogenesis in mice at cytogenetical, biochemical, histological and ultra-structural levels. SETTINGS AND DESIGN: To test if AA had a protective action against genotoxicity, cytotoxicity and tissue damage in liver during p-dimethylaminoazobenezene (p-DAB) induced hepatocarcinogenesis in mice, a group of mice were chronically fed 0.06% p-DAB and 0.05% phenobarbital (PB) for a varying period of time (7, 15, 30, 60, 90 and 120 days). A sub-group of the p-DAB plus PB fed mice were also fed 1% L-ascorbic acid. Several assays were periodically conducted (at the six intervals of fixation) for determination of genotoxic (based on chromosomal, nuclear and sperm head anomalies), cytotoxic (based on the marker enzymes aspartate transaminase; AST, alanine aminotransferase; ALT; acid phosphatase; ACP; alkaline phosphatase; ALKP; lipid peroxidation; LPO); and tissue damaging (based on optical and electron microscopic studies of liver at day 60 only) effects in these different groups of mice as compared to normal healthy control. METHODS AND MATERIAL: Adult healthy mice of Swiss Albino strain, reared and maintained in the animal house of the Department of Zoology, Kalyani University, under supervision of Animal Welfare Committee (which oversees ethical issues), served as materials for the present study. Widely practiced standard technique has been followed for each protocol. STATISTICAL ANALYSIS USED: The significance test between different series of data was conducted by student's t-test. RESULTS AND CONCLUSIONS: The results of all these studies indicated that AA had protective action against p-DAB induced hepatocarcinogenesis in mice.

Protein methylation in cellular proliferation and differentiation: Non-histone nuclear methyl acceptor protein(s) during 3'-methyl-4-dimethylaminoazobenzeneinduced hepatocarcinogenesis

An accelerating effect of methyl-deficient diet (MDD) on hepatocarcinogenesis and methylation pattern of nuclear protein(s) by S-adenosylmethionine: protein arginine N-methyltransferase (protein methylase I, PM-I) have been studied with 3'-methyl-4-dimethyl- aminoazobenzene(MeDAB)-treated rats. The MDD+MeDAB-fed group produced typical cancer cells in the liver almost two weeks earlier than the control synthetic diet (CSD)+MeDAB-fed group. Protein methylase I (PM-I) activity in the livers of MDD alone fed rats began to increase at around 2 weeks after MDD-feeding, reaching a peak at 4 weeks and declining thereafter. When nuclei isolated either from normal livers or from cholangiocarcinoma cells were incubated with PM-I preparation from normal liver, 16 and 23-kDa nuclear proteins were the major methylated proteins, regardless of the source of the nuclei. However, when the above mentioned nuclei were incubated with PM-I preparations either from MDD alone fed livers or MDD+ MeDAB-induced cholangiocarcinoma cells, the methylation of 23-kDa protein was not detected. The result suggests that there is a hitherto-unknown PM-I specific to 23 kDa nuclear protein which was lost during methyl deficient diet feeding and hepatocarcinogenesis. The N-terminal 20 amino acids sequence of the 23-kDa protein was found to be (1)Gly-Val-Pro-Leu-(5)X-Arg-Leu-Phe-Asp-(10)His-Ala-Met-Leu-Gln-(15)Ala -His-Arg-Ala-His-(20)Glu, having 94.7% sequence homology with human chorionic somatomammotropin precursor A and B.

Studies on rat liver nuclear DNA damaged by chemical carcinogen (3'-Me DAB) and AP DNA endonuclease. I. Purification and some properties of AP DNA endonucleases in rat liver chromatin

Three kinds of apurinic/apyrimidinic (AP) DNA endonuclease, APcI, APcII, APcIII, were purified from rat liver chromatin through 1M KCl extraction, DEAE-trisacryl ion exchange chromatography. Sephadex G-150 gel filtration and AP DNA cellulose affinity chromatography. Activities of the purified APcI, APcII and APcIII were 62.5, 83.3 and 52.0 EU/mg of protein, respectively. Molecular weights of APcI, APcII and APcIII, each consisting of a single polypeptide, were 30,000, 42,000 and 13,000, and isoelectric points of them were 7.2, 6.3 and 6.2, respectively. Three enzymes showed different substrate specificities; APcI acted only on AP DNA, and APcII acted on both AP DNA and UV DNA, while APcIII acted on 3'-methyl-4-monomethylaminoazobenzene (3'-Me MAB) DNA adduct as well as AP DNA and UV DNA. These results indicate that three kinds of AP DNA endonuclease present in rat liver chromatin have structural and functional diversities.

MRC-5 línea celular diploide como un modelo para el estudio fármacos con potencialidad carcinogénica / MRC-5 a diploid cellular line as a model for studying potencially carcinogenic drugs

Se evalúa el daño inducido al DNA de células humanas diploides MRC-5 por los siguientes carcinógenos: Benzo (a) pireno (Bp), 9-10 Dimetil, 1, 2, benzantraceno (Bz), 3 Metilcolantreno (Mc) metronidazol (met). El Bp, Bz y Mc produjeron modificaciones en el crecimiento celular, cambios en los cromosomas y cambios morfológicos que se han relacionado con la producción de neoplasias. ElMet no produce cambios en el patrón de crecimiento asociado a neoplasia, comportandose con un inhibidor del crecimiento celular. Creemos que para considerar a un agente químico como potencialmente carcinógeno, debe modificar en patrón de crecimiento con cambios en los cromosomas y modificaciones morfológicas. Este método de cultivo de tejidos tiene importancia como un sistema de cernimiento farmacológico permitiendo el estudio de un gran número de fármacos a un costo relativamente bajo

A Study of the Regulation of the Glucose Transporter in the Plasma Membranes of Hepatoma Cells Induced by 3'-Me DAB

5'-nucelotidase and glucose-6-phosphatase are liver plasma and microsomal membranes markers and their respective activities were determined. In the liver homogenate, the activities of 5'-nucleotidase were 0.58 +/- 0.08 and 0.29 +/- 0.07 micromols/mg protein/10min in the control and 3'-methyl-4-dimethyl aminoazobenzene (3'-Me DAB) groups respectively. The enzyme activities m the partially purified plasma membranes were 2.15 +/- 0.25 and 1.31 +/- 0.23 micromols/mg protein/10min in the control and 3'-Me DAB groups respectively. The glucose-6-phosphatase activities in the homogenates of the control and 3'-Me DAB groups were 0.23 +/- 0.10, and 0.45 +/- 0.25 micromols/mg protein/10min, and in the microsomal fraction, 1.14 +/- 0.32, and 0.63 +/- 0.11 micromols/mg protein/10min, respectively, The concentrations of glucose carrier in the plasma membranes from the control and 3'-Me DAB group were 25, and 35 pmols/mg membrane protein, respectively, and the Ka values for cytochalsin B in each group were 5.20 X 109. and 5.14 X 109ml/mol, respectively. However in the microsomal fraction, no significant differences of glucose carrier were found between the control and 3'-Me DAB groups from the DEAE Sephadex A-50 ion exchange chromatography, fractions I and ll were obtained. Electrophoretic analysis of fraction I revealed a major protein band with a molecular weight of 45,000 and minor bands with MWs of 50,000, 55,000 and 15,000. Following AcA 34 gel filtration, a major protein band with a MW of 45,000 was obtained. From these results, it can be concluded that the glucose carrier protein was increased on plasma membrane of hepatoma induced by 3'-Me DAB, and the carrier protein showed similar molecular weight to other glucose carrier found in the RBC, muscle cells and adipocyte.

Effect of p-Dimethylaminoazobenzene and 2(3)-tert-Butyl-4-hydroxyanisole on Lipid Pcroxidation, Glutathione-S-transferase, Peroxidase and Reductase in Rat Liver

An experiment was conducted in order to investigate the effect of p-dimethylaminoazobenzene (DAB) and 2(3)-tert-butyl-4-hydroxyanisole (BHA) on the lipid peroxidation and peroxide-destroying enzyme system in the rat liver. Dietary supplementation of DAB (0.06%) for three weeks caused the elevation of glutathione-S-transferase activity by 60% and glutathione reductase by 50%, but it decreased glutathione peroxidase and catalase activities significantly. Dietary supplementation of BHA (0.75%) also increased glutatione-S-transferase activity in the liver by 2 folds, and it counteracts DAB effect on the glutathione peroxidase and catalase activities. There was a marked increase in malon-dialdehyde content in the postnuclear fraction of liver by the treatment of DAB, but the addition of BHA lowered the malondialdehyde content to almost the control level. The protective effect of BHA on the lipid peroxidation induced by DAB administration at the enzyme level seems to be due to the induction of glutathione-S-transferase and the protection of glutathione peroxidase and catalase activities from being lowered by DAB administration.