[lean Production And Psychosocial Risks: The Case Of A Multinational Merger In A Metallurgical Company In Brazil].

This study focused on the method known as lean production as a work-related psychosocial risk factor in a Brazilian multinational auto parts company after its merger with other multinational companies. The authors conducted a qualitative analysis of two time points: the first using on-site observation and key interviews with managers and workers during implementation of lean production in 1996; the second, 16 years later, comparing data from a document search in labor inspection records from the Ministry of Labor and Employment and legal proceedings initiated by the Office of the Public Prosecutor for Labor Affairs. The merger led to layoffs, replacements, and an increase in the workday. A class action suit was filed on grounds of aggravated working conditions. The new production model led to psychosocial risks that increased the need for workers' health precautions when changes in the production process introduced new and increased risks of physical and mental illnesses.

Investigation Of Genetic Factors Underlying Typical Orofacial Clefts: Mutational Screening And Copy Number Variation.

Typical orofacial clefts (OFCs) comprise cleft lip, cleft palate and cleft lip and palate. The complex etiology has been postulated to involve chromosome rearrangements, gene mutations and environmental factors. A group of genes including IRF6, FOXE1, GLI2, MSX2, SKI, SATB2, MSX1 and FGF has been implicated in the etiology of OFCs. Recently, the role of the copy number variations (CNVs) has been studied in genetic defects and diseases. CNVs act by modifying gene expression, disrupting gene sequence or altering gene dosage. The aims of this study were to screen the above-mentioned genes and to investigate CNVs in patients with OFCs. The sample was composed of 23 unrelated individuals who were grouped according to phenotype (associated with other anomalies or isolated) and familial recurrence. New sequence variants in GLI2, MSX1 and FGF8 were detected in patients, but not in their parents, as well as in 200 control chromosomes, indicating that these were rare variants. CNV screening identified new genes that can influence OFC pathogenesis, particularly highlighting TCEB3 and KIF7, that could be further analyzed. The findings of the present study suggest that the mechanism underlying CNV associated with sequence variants may play a role in the etiology of OFC.