Search

Aim We report four cases of acquired severe encephalopathy with massive hyperkinesia, marked neurological and cognitive regression, sleep disturbance, prolonged mutism, and a remarkably delayed recovery (time to full recovery between 5 and 18mo) with an overall good outcome, and its association with anti-N-methyl-d-aspartate (anti-NMDA) receptor antibodies. Method We reviewed the four cases retrospectively and we also reviewed the literature. Results Anti-NMDA receptor antibodies (without ovarian teratoma detected so far) were found in the two children tested in this study. Interpretation The clinical features are similar to those first reported in 1992 by Sebire et al.,(1) and rarely recognized since. Sleep disturbance was not emphasized as part of the disorder, but appears to be an important feature, whereas coma is less certain and difficult to evaluate in this setting. The combination of symptoms, evolution (mainly seizures at onset), severity, paucity of abnormal laboratory findings, very slow recovery, and difficult management justify its recognition as a specific entity. The neuropathological substrate may be anatomically close to that involved in encephalitis lethargica, in which the same target functions (sleep and movement) are affected but in reverse, with hypersomnolence and bradykinesia. This syndrome closely resembles anti-NMDA receptor encephalitis, which has been reported in adults and is often paraneoplastic. [ABSTRACT FROM AUTHOR]

Background: Disparities in exposure to occupational hazards may be linked to social position as well as the type of job a person holds. This study aimed to describe the prevalence of exposure to workplace hazards among three migrant worker groups and to assess whether social disparities in exposure for these groups remain after adjusting for occupational characteristics., Methods: Data were collected in 2017/2018 from 1630 Australian workers born in New Zealand, India, and the Philippines. Weighted estimated prevalence of exposure to 10 carcinogens and four psychosocial hazards (discrimination, job strain, vulnerability, and insecurity) was calculated for sociodemographics and occupation. Regression estimated the likelihood of exposure by sociodemographics after adjustment for occupational characteristics., Results: Exposure to workplace hazards ranged from 11.7% (discrimination) to 61.2% (exposed to at least one carcinogen). Compared with workers born in India, New Zealand born workers were over twice as likely to be exposed to diesel engine exhaust (adjusted odds ratio [aOR] = 2.60) and 60% more likely to be exposed to at least one carcinogen (aOR = 1.60) but less likely to be exposed to any psychosocial hazard. Social disparities by country of birth, sex, age, education, and number of years in Australia, as well as company size, employment type, and hours, worked remained associated with greater likelihood of reporting one or more workplace hazards after adjusting for occupational characteristics., Conclusion: Examining sociodemographic as well as occupational characteristics helps to clarify groups most likely to be exposed to workplace hazards who can be hidden when examining occupational characteristics alone., (© 2020 Wiley Periodicals LLC.)

Tumor necrosis factor (TNF) plays a critical role in pathomechanisms associated with secondary damage after traumatic brain injury (TBI). The TNF ligand-receptor system stimulates inflammation by activation of gene transcription through the IkappaB kinase (IKK)-NF-kappaB and c-Jun NH(2)-terminal kinase (JNK)-AP-1 signaling cascades. TNF signaling following TBI involves both cell survival and apoptotic pathways, but the mechanism that accounts for the dual role of TNF remains unclear. Multiple studies have reported hypothermia to be protective following TBI, but the precise mechanism has not been clearly defined. Here, TNFR1 signaling pathways were investigated in the cerebral cortex of adult male Sprague-Dawley rats subjected to moderate fluid-percussion TBI and of naïve controls. Another group was subjected to moderate TBI with 30 min of pre- and post-traumatic hypothermia (33 degrees C). Rapid and marked increases in protein expression of TNFR1 and signaling intermediates in both the IKK-NF-kappaB and JNK pathways were induced in traumatized cortices. Hypothermia decreased TNFR1 protein expression acutely in traumatized cortices and stimulated early activation of signaling intermediates in the JNK, but not the IKK-NF-kappaB, signaling pathways. Hypothermia promoted a rapid activation of caspase-3 acutely after injury but suppressed caspase-3 activation at later time points. Moreover, hypothermia treatment suppressed cleavage of X-linked inhibitor of apoptosis protein (XIAP) into fragments induced by TBI. These data suggest that hypothermia may regulate both the JNK signaling cascade via XIAP and the preconditioning pathways that activate caspases. Thus, hypothermia mediates TNFR1 responses via early activation of the JNK signaling pathway and caspase-3, leading to endogenous neuroprotective events.