Improvement of quality of life after therapeutic plasma exchange in patients with myasthenic crisis

Introduction We sought to evaluate quality of life patients with myasthenic crisis before and after therapeutic plasma exchange. Materials and methods In our study we conducted an assessment of the quality of life with the use of the questionnaire SF-36, when executed eleven therapeutic plasma exchange. The assessment was made on baseline and after 4 weeks. We also did neurological clinical evaluation before and after TPE. Results Patients in the study showed significant improvement in quality of life after performed therapeutic plasma exchange. The changes were observed in physical functioning, which confirmed the results of the statistical significance of p<0.05. In the analysis, the assessment of mental functioning not obtained the results of statistical significance, but the results also showed improvement in self-assessment. We observed high correlation between general health and physical mental functioning, between the role limitations due to physical health problems and role limitations due to emotional problems, and general health perception and bodily pain. Conclusions Therapeutic plasma exchange significantly improves the quality of life of patients with myasthenia gravis during the crisis

Lessons on brain edema in HE : from cellular to animal models and clinical studies

Brain edema is considered as a common feature associated with hepatic encephalopathy (HE). However, its central role as cause or consequence of HE and its implication in the development of the neurological alterations linked to HE are still under debate. It is now well accepted that type A and type C HE are biologically and clinically different, leading to different manifestations of brain edema. As a result, the findings on brain edema/swelling in type C HE are variable and sometimes controversial. In the light of the changing natural history of liver disease, better description of the clinical trajectory of cirrhosis and understanding of molecular mechanisms of HE, and the role of brain edema as a central component in the pathogenesis of HE is revisited in the current review. Furthermore, this review highlights the main techniques to measure brain edema and their advantages/disadvantages together with an in-depth description of the main ex-vivo/in-vivo findings using cell cultures, animal models and humans with HE. These findings are instrumental in elucidating the role of brain edema in HE and also in designing new multimodal studies by performing in-vivo combined with ex-vivo experiments for a better characterization of brain edema longitudinally and of its role in HE, especially in type C HE where water content changes are small

Lessons on brain edema in HE: from cellular to animal models and clinical studies

Brain edema is considered as a common feature associated with hepatic encephalopathy (HE). However, its central role as cause or consequence of HE and its implication in the development of the neurological alterations linked to HE are still under debate. It is now well accepted that type A and type C HE are biologically and clinically different, leading to different manifestations of brain edema. As a result, the findings on brain edema/swelling in type C HE are variable and sometimes controversial. In the light of the changing natural history of liver disease, better description of the clinical trajectory of cirrhosis and understanding of molecular mechanisms of HE, and the role of brain edema as a central component in the pathogenesis of HE is revisited in the current review. Furthermore, this review highlights the main techniques to measure brain edema and their advantages/disadvantages together with an in-depth description of the main ex-vivo/in-vivo findings using cell cultures, animal models and humans with HE. These findings are instrumental in elucidating the role of brain edema in HE and also in designing new multimodal studies by performing in-vivo combined with ex-vivo experiments for a better characterization of brain edema longitudinally and of its role in HE, especially in type C HE where water content changes are small

Abnormal brain oxygen homeostasis in an animal model of liver disease

Background & Aims: Increased plasma ammonia concentration and consequent disruption of brain energy metabolism could underpin the pathogenesis of hepatic encephalopathy (HE). Brain energy homeostasis relies on effective maintenance of brain oxygenation, and dysregulation impairs neuronal function leading to cognitive dysfunction. We hypothesise that HE is associated with reduced brain oxygenation and explored the potential role of ammonia as an underlying pathophysiological factor. / Methods: In a rat model of chronic liver disease with minimal HE (mHE; bile duct ligation [BDL]), brain tissue oxygen measurement and proton magnetic resonance spectroscopy were used to investigate how hyperammonemia impacts oxygenation and metabolic substrate availability in the CNS. Ornithine phenylacetate (OP, OCR-002; Ocera Therapeutics, USA) was used as an experimental treatment to reduce ammonia concentration in plasma. / Results: In BDL animals, glucose, lactate and tissue oxygen concentrations in the cerebral cortex were significantly lower compared to sham-operated controls. OP treatment corrected the hyperammonemia and restored brain tissue oxygen. While BDL animals were hypotensive, cortical tissue oxygen was significantly improved by treatments which increased arterial blood pressure. Cerebrovascular reactivity to exogenously applied CO2 was found to be normal in BDL animals. / Conclusions: These data suggest that hyperammonemia significantly decreases cortical oxygenation, potentially compromising brain energy metabolism. These findings have potential clinical implications for the treatment of patients with mHE aiming to restore normal brain blood flow alongside ammonia-reducing strategies

Multi-functional magnetic photoluminescent photocatalytic polystyrene-based micro- and nano-fibers Obtained by electrospinning

This work reports on the implementation of electrospinning (ES) as a facile route to encapsulate nano-engineered materials in a polystyrene (PS) matrix. We applied ES to co-encapsulate two kinds of nanoparticles, i.e., upconversion nanophosphors (UCNPs) and superparamagnetic iron oxide nanoparticles (SPIONs), in polystyrene (PS)-based micro- and nano-fibers (PSFs). This approach made it possible to integrate near-infrared (NIR) light-sensitive 500-nm β-NaYF₄:Yb, Er UCNPs with 10-nm γ-Fe₂O₃ SPIONs in PS fibers. During the ES process, PSFs were additionally loaded with a well-established singlet oxygen (¹∆g) photosensitizer, rose bengal (RB). The thus obtained PSFs revealed the promising features of prospective multi-functional magnetic photoluminescent photocatalytic nano-constructs

Photocatalytic and phototoxic properties of TiO2-based nanofilaments: ESR and AFM assays

There is uncertainty in understanding of the relationship between physico-chemical parameters of nanosized titanium dioxide (nano-TiO2) and its toxicity when brought into contact with living cells. This study provides a multidisciplinary experimental insight into the toxicity and phototoxicity of the custom-made TiO2-based nanowires (TiO2-NWs). We employed electron spin resonance (ESR) to detect reactive oxygen species (ROS) generated in aqueous suspensions of TiO2-NWs and combined these results with atomic force microscopy (AFM) to trace the onset of toxic effects towards human melanoma cells. The cells were treated with low concentrations (similar to 2.5 mu g/ml) of TiO2-NWs and Degussa P25. High-resolution AFM surface topography and cell elasticity measurements revealed toxic effects both in cells incubated with TiO2-NWs in the dark and exposed to the photo-oxidative stress under UVA radiation. In contrast to ROS generation efficacy in the absence of cells in vitro, no direct correlation was found between the physical parameters of nano-TiO2 and cell toxicity

Atom-Transfer Radical Addition Reactions Catalyzed by RuCp* Complexes: A Mechanistic Study

Kinetic and spectroscopic analyses were performed to gain information about the mechanism of atom-transfer radical reactions catalyzed by the complexes [RuCl2Cp*(PPh3)] and [RuClCp*(PPh3)2] (Cp*=pentamethylcyclopentadienyl), in the presence and in the absence of the reducing agent magnesium. The reactions of styrene with ethyl trichloroacetate, ethyl dichloroacetate, or dichloroacetonitrile were used as test reactions. The results show that for substrates with high intrinsic reactivity, such as ethyl trichloroacetate, the oxidation state of the catalyst in the resting state is +3, and that the reaction is zero-order with respect to the halogenated compound. Furthermore, the kinetic data suggest that the metal catalyst is not directly involved in the rate- limiting step of the reaction