The hepatic stellate (Ito) cell lies within the space of Disse and has a variety of functions. Stellate cells store vitamin A in characteristic lipid droplets. In the normal human liver, the cells can be identified by the presence of these lipid droplets; in addition, many stellate cells in the normal liver express alpha-smooth muscle actin. In acute liver injury, there is an expansion of the stellate cell population with increased alpha-smooth muscle actin expression; stellate cells appear to play a role in extracellular matrix remodelling after recovery from injury. In chronic liver injury, the stellate cell differentiates into a myofibroblast-like cell with marked expression of alpha-smooth muscle actin and occasional expression of desmin. Myofibroblast-like cells have a high fibrogenic capacity in the chronically diseased liver and are also involved in matrix degradation. In vitamin A intoxication, hypertrophy and proliferation of the stellate and myofibroblast-like cells may lead to non-cirrhotic portal hypertension, fibrosis and cirrhosis. In liver tumours, myofibroblast-like cells are involved in the capsule formation around the tumour and in the production of extracellular matrix within it. The transition of stellate cells into myofibroblast-like cells is regulated by an intricate network of intercellular communication between stellate cells and activated Kupffer cells, damaged hepatocytes, platelets, endothelial and inflammatory cells, involving cytokines and nonpeptide mediators such as reactive oxygen species, eicosanoids and acetaldehyde. The findings suggest that the stellate cell plays an active role in a number of human liver diseases, with a particular reactivity pattern in fibrotic liver disorders.

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Prison employees are often confronted with critical incidents and chronic stressors that may lead to trauma or burnout symptoms. However, most of the research on clinical aspects of interpersonal violence in prisons (inmates-to-staff violence, specifically) focuses either on trauma or on burnout. The purpose of the present study is (a) to examine both burnout and posttraumatic stress among prison staff and (b) to examine the influences of inmates-to-staff violent relations on posttraumatic stress in terms of risk profile to develop PTSD. A random sample of French correctional employees has completed various self-reported questionnaires assessing burnout, posttraumatic stress, and stress as well as victimization and demographic characteristics. Correctional employees demonstrated high levels of PTSD symptoms, burnout, and stress. Violent interactions with inmates lead to experienced trauma of all types (PTSD, secondary, or vicarious trauma). Results have highlighted a prison worker's profile prone to PTSD: he or she expresses high levels of emotional exhaustion, intense levels of stress, high levels of depersonalization, and high levels of intrusion, avoidance, and hyperreactivity. This study contributes to an understanding of the literature by explaining the complex association between burnout and posttraumatic stress after interpersonal violence. These findings suggest a need to support prison workers and to address inmates-to-staff relational dynamics.

We conducted a case-control study in five general hospitals in the region of Antwerp, studying 161 patients (102 men, 59 women) and hospital control subjects matched for age and sex to explore the relation between drug use and upper gastrointestinal bleeding from 'erosive lesions' (peptic oesophagitis, gastric erosions, gastric ulcer(s), or duodenal ulcer(s)).There was a highly significant difference between cases and control subjects in the use of non-steroidal anti-inflammatory drugs (NSAIDs, excluding aspirin) (odds ratio 7.4, p<000l; 95% confidence interval odds ratio 3.7 to 14.7). There also was a significant difference in the use of aspirin (odds ratio 2.2, p=0.025; 95% CI odds ratio 1.3 to 4.0) and a highly significant difference regarding the presence of antecedents of peptic ulcer disease (odds ratio 5.5, p<0.001; 95% CI odds ratio 3.2 to 9.6). There was no significant difference in the use of other drugs, paracetamol and corticosteroids in particular, nor in the use of alcohol or tobacco. The patient group using NSAIDs was older, had more women, and had a higher mortality than the group not using NSAIDs. Among patients with bleeding gastric or duodenal ulcer(s), NSAID users were not more or less likely to have had symptoms of peptic ulcer disease, and had no higher frequency of multiple gastric or duodenal ulcers. The attributable risk for NSAID use was 030 (95% CI 0.23 to 0.37) and for aspirin use 0.14 (95% CI 0-08 to 0.20).

The term "microvesicular steatosis of the liver" refers to a variant form of hepatic fat accumulation whose histologic features contrast with the much more common macrovesicular steatosis. Microvesicular steatosis of the liver was originally described in association with conditions who share a number of biochemical and a limited number of clinical features: acute fatty liver of pregnancy, Reye's syndrome, Jamaican vomiting sickness, sodium valproate toxicity, high-dose tetracycline toxicity and certain congenital defects of urea cycle enzymes; they were thought to constitute an entity of "microvesicular fat diseases". In recent years the disease has been described in a wide variety of conditions: alcoholism, toxicity of several medications, delta hepatitis in South America and Central Africa, sudden childhood death, congenital defects of fatty acid beta oxidation, cholesterol ester storage disease, Wolman disease and Alpers syndrome. Not much is known regarding the pathogenesis of microvesicular steatosis but in many instances the primary defect could be a mitochondrial lesion, and inhibition of the mitochondrial beta oxidation of fatty acids has been the most frequently implicated defect. The different conditions associated with microvesicular steatosis are heterogenous in many aspects. Maintaining the concept of "microvesicular fat diseases" as a unique entity seems no longer justified.