Development of a Personal Ultrasound Exposimeter for Occupational Health Monitoring.

Prolonged exposure to airborne ultrasound in a workplace can have a detrimental influence on a worker's well-being. Given the ever-increasing use of ultrasonic industrial equipment, it is of vital importance-and may also be regulated by law-to monitor ultrasound exposure during a normal workday as part of workplace risk assessment. However, the devices currently utilized exhibit limitations with regard to both their operational frequency and their portability (wearability). In this paper, the first prototype of a high-frequency and ultrasound personal exposimeter is presented in the light of the latest national and international standards governing high-frequency and ultrasonic noise measurement in the field of occupational health monitoring. The prototype was tested in the laboratory environment in order to assess its sound level detection capabilities in both the audible and ultrasonic frequency ranges. Several common industrial scenarios-including an ultrasonic welding machine, an ultrasonic cleaning bath, and a compressed air gun-were simulated in a laboratory environment. For each simulated set-up, a corresponding high-frequency or ultrasonic signal was fed through a specially prepared generation chain. Each experimental scenario was initially surveyed with an ultrasound level meter previously tested up to 100 kHz. This was followed by a measurement with the prototype. For this study, the simulated sound signals varied between 10 kHz and 40 kHz on the frequency scale and between 60 dB and 90 dB in amplitude. The portability of the prototype, which may be required to be worn throughout an entire workday (e.g., 8 h), was also considered. All the experiments were performed on a customized ultrasound measurement set-up within a free-field environment located at the Physikalisch-Technische Bundesanstalt (PTB) in Braunschweig, Germany. Results obtained suggest a good agreement between the measurements performed with both devices in the louder areas of the sound fields produced. Because the overall measurement uncertainty is highly dependent on the specificity of the individual measurement set-up and measurement procedure, an uncertainty budget estimated for the prototype considers electro-acoustical contributions only.

Role of pro-inflammatory cytokines of pancreatic islets and prospects of elaboration of new methods for the diabetes treatment.

Several relations between cytokines and pathogenesis of diabetes are reviewed. In type 1 and type 2 diabetes an increased synthesis is observed and as well as the release of pro-inflammatory cytokines, which cause the damage of pancreatic islet cells and, in type 2 diabetes, the development of the insulin resistance. That process results in the disturbed balance between pro-inflammatory and protective cytokines. Pro-inflammatory cytokines such as interleukin 1ß (IL-1ß), tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), as well as recently discovered pancreatic derived factor PANDER are involved in the apoptosis of pancreatic ß-cells. Inside ß-cells, cytokines activate different metabolic pathways leading to the cell death. IL-1ß activates the mitogen-activated protein kinases (MAPK), affects the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and activates the inducible nitric oxide synthase (iNOS). TNF-α and IFN-γ in a synergic way activate calcium channels, what leads to the mitochondrial dysfunction and activation of caspases. Neutralization of pro-inflammatory cytokines, especially interleukin 1ß with the IL-1 receptor antagonist (IL-1Ra) and/or IL-1ß antibodies might cause the extinction of the inflammatory process of pancreatic islets, and consequently normalize concentration of glucose in blood and decrease the insulin resistance. In type 1 diabetes interleukin-6 participates in regulation of balance between Th17 and regulatory T cells. In type 2 diabetes and obesity, the long-duration increase of IL-6 concentration in blood above 5 pg/ml leads to the chronic and permanent increase in expression of SOCS3, contributing to the increase in the insulin resistance in cells of the skeletal muscles, liver and adipose tissue.

Relationship between the induction of inflammatory processes and infectious diseases in patients with ischemic stroke.

Pro-inflammatory cytokines participate in the induction of ischemic stroke. So far, their participation in the cerebral ischemia was proven for the tumor necrosis factor TNF-α, interleukin-1 (IL-1), and interleukin-6 (IL-6). The release of the pro-inflammatory cytokines into the extracellular space causes the enlargement of the brain damage region, and consequently increases the neurological deficit and negatively affects the survival rate prognoses. That is confirmed by the increased concentration of pro-inflammatory cytokines in blood and the cerebrospinal fluid of patients with brain stroke, as well as by the research on the induced/experimental cerebral ischemia in animals. The pro-inflammatory cytokines participate in the migration of the reactive T lymphocytes to the regions of brain ischemia where they enhance the nerve tissue damage by down-regulation of microcirculation, induce the pro-thrombotic processes and release other neurotoxic cytokines. Also, in the early stage of cerebral ischemia, cytokines activate the axis hypothalamus-pituitary gland-adrenal cortex and increase the cortisol concentration in blood, what results in the decreased resistance to infectious diseases. Administration of the inhibitor of the interleukin-1 receptor (IL-1Ra) inhibits the inflammatory processes in the region of brain ischemia, and subsequently improves the prognosis for the size of the neurological deficit and the survival rate, as well as resistance to infectious diseases.