Legal issues in accidents caused by sleepiness

The impact of shift-work on sleep, performance and general health appears to be substantial. The most immediate consequence of night shiftwork is sleep loss. The aim of the present paper is to describe legal cases involving accidents attributed to sleepiness or fatigue, mainly as a consequence of shift-work or prolonged work hours, in the UK, USA and Australia. The paper will describe how legal systems are dealing with such incidents and how this may change in the future. Accidents related to sleepiness may result in criminal prosecution, for example charges of culpable driving. For acts performed while a person is sleeping (e.g., motor vehicle accidents), the legal question of voluntariness may be raised. The issue of employers' liability in such cases is contentious. Special liability regimes are in place to cover employers' liability. Employers may be deemed liable for injuries of third parties caused by wrongful acts of employees committed in the course of their employment. In the future, it is likely that employers will need to take greater precautions to reduce sleepiness and fatigue in the workplace, especially where the risk to public and environmental safety, health and productivity are significant.     

Selected organopathies caused by experimental magnesium deficiency

A role of enzyme mediated metabolic processes is discussed. Unfavourable effect of magnesium deficiency on the functioning of various organs may lead to extensive and irreversible morphological changes of focal character. Basing on the results of several experiments and own experience, the author discusses an effect of low-magnesium diet on histological, histochemical, and microscopic lesions to the myocardium, skeletal musculature, liver, and pancreas. Magnesium deficiency predisposes to myocardial necrosis which simulates electrolyte-steroid-cardiomyopathy by necrosis (ESCN). Low-magnesium diet decreases resistance of the animals to various types of stress such as: cooling, immobilization, and noise. Insignificant degree of the lesions to skeletal musculature produced by magnesium deficiency and no progress in these lesions during the experiment may depend upon relatively stable magnesium reserve in the muscles. Low-magnesium diet increases the number of so-called Ito cells in the liver. It is probable that these cells together with hepatocytes contribute to the formation of collagen fibres. Magnesium deficiency may lead to the abnormal digestion of nutrients in the pancreas, interfering with exocytosis of zymogen granules. Supplementation of the diet with magnesium may prevent various organopathies.     

Enhanced ototoxicity of gentamicin and salicylate caused by Mg deficiency and Zn deficiency

In rats, Mg deficiency caused a moderate hearing loss, measured by means of evoked potentials at 10 and 20 kHz, which was repaired after refeeding a normal diet. Application of 700 mg/kg salicylic acid or injection of 5×100 mg/kg gentamicin also caused a reversible hearing loss in normally fed rats. Treatment of Zn-deficient rats with salicylic acid produced a stronger although reversible hearing loss than in normally fed salicylate-treated rats. Treatment of Mg-deficient rats with gentamicin induced a strong hearing loss that was nearly complete and irreversible in 9 of 25 rats.     

Zinc deficiency aggravates tubulointerstitial nephropathy caused by ureteral obstruction

Ureteral ligation causes tubulointerstitial nephropathy characterized by the tubular dilatation, the interstitial expansion, and a leukocyte infiltration into the tubulointerstitium. The present study was designed to explore whether zinc (Zn) deficiency affects the development of unilateral ureteral obstruction (UUO)-induced tubulointerstitial nephropathy. Compared to rats fed a standard diet, rats fed a Zn-deficient diet exhibited a greater influx of leukocytes into the tubulointerstitium of the cortex of the obstructed kidney 3 d following UUO. Furthermore, rats fed a Zn-deficient diet showed a slight invasion of leukocytes into the tubulointerstitium of the cortex of the contralateral nonobstructed kidney (CLK), although there was no infiltration of leukocytes into the CLK of rats fed a standard diet. These histological changes, however, were ameliorated by administration of enalapril, an angiotensin (ANG) I-converting enzyme inhibitor. Thus, it is suggested that Zn deficiency aggravates UUO-induced tubulointerstitial nephropathy via an increase in the action of ANG II.     

Mast cells rescue implantation defects caused by c-kit deficiency

Various physiologically relevant processes are regulated by the interaction of the receptor tyrosine kinase (c-Kit) and its ligand stem cell factor (SCF), with SCF known to be the most important growth factor for mast cells (MCs). In spite of their traditional role in allergic disorders and innate immunity, MCs have lately emerged as versatile modulators of a variety of physiologic and pathologic processes. Here we show that MCs are critical for pregnancy success. Uterine MCs presented a unique phenotype, accumulated during receptivity and expanded upon pregnancy establishment. Kit^W-sh/W-sh mice, whose MC deficiency is based on restricted c-Kit gene expression, exhibited severely impaired implantation, which could be completely rescued by systemic or local transfer of wild-type bone marrow-derived MCs. Transferred wild-type MCs favored normal implantation, induced optimal spiral artery remodeling and promoted the expression of MC proteases, transforming growth factor-β and connective tissue growth factor. MCs contributed to trophoblast survival, placentation and fetal growth through secretion of the glycan-binding protein galectin-1. Our data unveil unrecognized roles for MCs at the fetomaternal interface with critical implications in reproductive medicine.     

Iron deficiency caused by 7 weeks of intensive physical exercise

The present study was designed to evaluate the effect of an intensive physical training program involving both isometric and isotonic activities on the body iron status of 8 females and 11 males (age 20 +/- 1 year). The training was carried out over a 7 week period and included 8 h of varying physical activities each day. Venous blood samples were obtained from the subjects prior to the beginning of the training, on day 2 and in weeks 2, 4, 6 and 7 of the program. Blood samples were analyzed for iron, ferritin and hemoglobin (Hb) concentrations, total iron binding capacity (TIBC) and red blood cell count (RBC). Iron levels of males and females decreased 65% after 2 weeks of training (p less than 0.001). At the end of the training program 5 males and 6 females had lower than normal iron values (less than 13.4 mumol.l-1). TIBC increased 25% in women and 18% in men following 2 and 4 weeks of training (p less than 0.001) and remained at this elevated level throughout the training period. Ferritin levels decreased 50% in both sexes after 4 weeks of exercise (p less than 0.05) and remained at this level until the end of the training. Hb and RBC decreased 8-10% in both sexes during the training period. In two of the women anemia occurred after 4 weeks of training. The development of latent iron deficiency in a substantial number of participants after a relatively short period of training is uncommon and may reflect the high intensity of exercise required in this program.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alternative explanation for excision repair deficiency caused by the polAex1 mutation

An investigation of the mechanism of the polAex1 mutation in vitro suggested that the excision repair deficiency observed in vivo does not result from an inability of the enzyme to nick translate. The defect appears to reside in the inability of the enzyme to effectively generate a nick structure to serve as a substrate for DNA ligase.