Effect of a skin-deep surface zone on formation of two-dimensional electron gas at a semiconductor surface

Two dimensional electron gases (2DEGs) at surfaces and interfaces of semiconductors are described straightforwardly with a 1D self-consistent Poisson-Schr\"{o}dinger scheme. However, their band energies have not been modeled correctly in this way. Using angle-resolved photoelectron spectroscopy we study the band structures of 2DEGs formed at sulfur-passivated surfaces of InAs(001) as a model system. Electronic properties of these surfaces are tuned by changing the S coverage, while keeping a high-quality interface, free of defects and with a constant doping density. In contrast to earlier studies we show that the Poisson-Schr\"{o}dinger scheme predicts the 2DEG bands energies correctly but it is indispensable to take into account the existence of the physical surface. The surface substantially influences the band energies beyond simple electrostatics, by setting nontrivial boundary conditions for 2DEG wavefunctions.Comment: 9 pages, 7 figures, 2 table

Distal biceps tendon rupture: a comprehensive overview

Distal biceps tendon (DBT) is a relatively rare injury mainly occurring in middle-aged men while in eccentric biceps muscle contraction. Clinical appearance with proximal avulsion of the muscle and specific clinical tests are most of the time sufficient for diagnosing DBT, but if needed ultrasonography and MRI, most often in FABS view, can be used to ensure diagnosis of DBT and partial DBT. Surgical anatomical reinsertion has shown to be a successful method of treatment, although conservative treatment can be initiated in older patients. Two different approaches are described in literature: single- and double-incision techniques with different fixation methods proving to have similarly good results. Major complications of surgical intervention are posterior interosseous nerve palsy and symptomatic heterotropic ossification. Overall outcome of surgical intervention has shown high subjective satisfaction with slight weakness in flexion and supination but mostly without loss in range of motion

An investigation of the kynurenine pathway in experimental arthritis

The kynurenine pathway is a catabolic biochemical pathway responsible for degradation of tryptophan, an essential amino acid. As a consequence, biologically active molecules, kynurenines, are produced. These chemical entities can influence immune responses. Previously, it has been shown that pharmacological inhibition of the initial step on the pathway increases the severity of collagen-induced arthritis (CIA), an animal model of rheumatoid arthritis. In contrast, treatment with kynurenine, a major by product of tryptophan degradation, effectively ameliorated the disease. This project was based around the hypothesis that tryptophan metabolism via the kynurenine pathway represents an endogenous regulatory mechanism that is activated in response to inflammation. To test this hypothesis, I carried out a comprehensive analysis of the kynurenine pathway in the immune system in CIA as well as in the liver or kidneys, organs in which kynurenine pathway is the most active under normal conditions. In this study, the endogenous activity of the kynurenine pathway in the immune system (lymph nodes and spleen), inflamed paws, liver, and kidneys was monitored during the induction phase of CIA (day 14 after immunisation) and during the period of disease resolution (day 10 after disease onset). In addition, the concentration of tryptophan, kynurenine and its selected catabolites anthranilic acid (AA) and 3-hydroxyanthranilic acid (3-HAA) was determined in the sera. All results were compared with naive tissues.Increased expression of all enzymes along the kynurenine pathway was observed locally in draining lymph nodes during the pre-arthritic phase of arthritis and this was accompanied by reduced levels of tryptophan. In contrast, during the resolution phase of arthritis not only was there decreased tryptophan concentration, but also there was an accumulation of the downstream tryptophan metabolites, kynurenine, AA, and 3-HAA in lymph nodes. In addition, the accumulation of kynurenine and its downstream metabolites observed during the resolution of arthritis was accompanied by reduced expression of enzymes involved in kynurenine catabolism (kynureninase, kynurenine 3-monooxygenase, and 3-hydroxyanthranilate 3,4 dioxygenase) towards the levels found in naïve mice. These findings provide for the first time evidence of an association between resolution of arthritis and the local accumulation of kynurenines in lymph nodes. However, in the paws and spleens of mice with CIA, there was no evidence of activation of the kynurenine pathway. Surprisingly, however, kynurenine catabolism was increased in the kidneys and liver during CIA which may explain why in sera from mice with CIA, the tryptophan concentration was not changed, whereas levels of kynurenine, AA, and 3-HAA actually decreased, despite the increased levels found in lymph nodes at the same time points. Based on these findings I assessed the potential therapeutic effect of exogenous administration of AA and 3-HAA in mice with established CIA and in order to facilitate this study I established a novel method of assessment of bone integrity based on 3-dimensional imaging using micro-computed tomography. Using in vivo observations, micro-computed tomography and histological sectioning with hematoxylin and eosin staining, I showed that neither AA nor 3-HAA treatment was effective in established CIA. However, treatment with etanercept, a potent inhibitor of TNF, profoundly reduced the severity of bone and cartilage damage. I also confirmed previous findings that tranilast, a derivative of 3-HAA which exhibits kynurenine-like activity and has a longer half-life than naturally occurring tryptophan metabolite, was effective in established CIA. Thus, taken together, activation of the kynurenine pathway in the lymph nodes may constitute a fine tuning mechanism involved in resolution of inflammation. However, exogenous administration of naturally occurring kynurenines is unlikely to be an effective therapeutic strategy to reduce inflammation in arthritis, possibly because of their rapid clearance from the circulation

An investigation of the kynurenine pathway in experimental arthritis

The kynurenine pathway is a catabolic biochemical pathway responsible for degradation of tryptophan, an essential amino acid. As a consequence, biologically active molecules, kynurenines, are produced. These chemical entities can influence immune responses. Previously, it has been shown that pharmacological inhibition of the initial step on the pathway increases the severity of collagen-induced arthritis (CIA), an animal model of rheumatoid arthritis. In contrast, treatment with kynurenine, a major by product of tryptophan degradation, effectively ameliorated the disease. This project was based around the hypothesis that tryptophan metabolism via the kynurenine pathway represents an endogenous regulatory mechanism that is activated in response to inflammation. To test this hypothesis, I carried out a comprehensive analysis of the kynurenine pathway in the immune system in CIA as well as in the liver or kidneys, organs in which kynurenine pathway is the most active under normal conditions. In this study, the endogenous activity of the kynurenine pathway in the immune system (lymph nodes and spleen), inflamed paws, liver, and kidneys was monitored during the induction phase of CIA (day 14 after immunisation) and during the period of disease resolution (day 10 after disease onset). In addition, the concentration of tryptophan, kynurenine and its selected catabolites anthranilic acid (AA) and 3-hydroxyanthranilic acid (3-HAA) was determined in the sera. All results were compared with naive tissues.Increased expression of all enzymes along the kynurenine pathway was observed locally in draining lymph nodes during the pre-arthritic phase of arthritis and this was accompanied by reduced levels of tryptophan. In contrast, during the resolution phase of arthritis not only was there decreased tryptophan concentration, but also there was an accumulation of the downstream tryptophan metabolites, kynurenine, AA, and 3-HAA in lymph nodes. In addition, the accumulation of kynurenine and its downstream metabolites observed during the resolution of arthritis was accompanied by reduced expression of enzymes involved in kynurenine catabolism (kynureninase, kynurenine 3-monooxygenase, and 3-hydroxyanthranilate 3,4 dioxygenase) towards the levels found in naïve mice. These findings provide for the first time evidence of an association between resolution of arthritis and the local accumulation of kynurenines in lymph nodes. However, in the paws and spleens of mice with CIA, there was no evidence of activation of the kynurenine pathway. Surprisingly, however, kynurenine catabolism was increased in the kidneys and liver during CIA which may explain why in sera from mice with CIA, the tryptophan concentration was not changed, whereas levels of kynurenine, AA, and 3-HAA actually decreased, despite the increased levels found in lymph nodes at the same time points. Based on these findings I assessed the potential therapeutic effect of exogenous administration of AA and 3-HAA in mice with established CIA and in order to facilitate this study I established a novel method of assessment of bone integrity based on 3-dimensional imaging using micro-computed tomography. Using in vivo observations, micro-computed tomography and histological sectioning with hematoxylin and eosin staining, I showed that neither AA nor 3-HAA treatment was effective in established CIA. However, treatment with etanercept, a potent inhibitor of TNF, profoundly reduced the severity of bone and cartilage damage. I also confirmed previous findings that tranilast, a derivative of 3-HAA which exhibits kynurenine-like activity and has a longer half-life than naturally occurring tryptophan metabolite, was effective in established CIA. Thus, taken together, activation of the kynurenine pathway in the lymph nodes may constitute a fine tuning mechanism involved in resolution of inflammation. However, exogenous administration of naturally occurring kynurenines is unlikely to be an effective therapeutic strategy to reduce inflammation in arthritis, possibly because of their rapid clearance from the circulation.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Agomelatine Changed the Expression and Methylation Status of Inflammatory Genes in Blood and Brain Structures of Male Wistar Rats after Chronic Mild Stress Procedure

The preclinical research conducted so far suggest that depression development may be influenced by the inflammatory pathways both at the periphery and within the central nervous system. Furthermore, inflammation is considered to be strongly connected with antidepressant treatment resistance. Thus, this study explores whether the chronic mild stress (CMS) procedure and agomelatine treatment induce changes in TGFA, TGFB, IRF1, PTGS2 and IKBKB expression and methylation status in peripheral blood mononuclear cells (PBMCs) and in the brain structures of rats. Adult male Wistar rats were subjected to the CMS and further divided into matched subgroups to receive vehicle or agomelatine. TaqMan gene expression assay and methylation-sensitive high-resolution melting (MS-HRM) were used to evaluate the expression of the genes and the methylation status of their promoters, respectively. Our findings confirm that both CMS and antidepressant agomelatine treatment influenced the expression level and methylation status of the promoter region of investigated genes in PBMCs and the brain. What is more, the present study showed that response to either stress stimuli or agomelatine differed between brain structures. Concluding, our results indicate that TGFA, TGFB, PTGS2, IRF1 and IKBKB could be associated with depression and its treatment

Influence of Environmental Factors and Relationships between Vanadium, Chromium, and Calcium in Human Bone

The aim of this study was to investigate the impact of environmental factors on the concentrations of vanadium (V), chromium (Cr), and calcium (Ca) and to examine the synergistic or antagonistic relationships between these metals, in cartilage (C), cortical bone (CB), and spongy bone (SB) samples obtained following hip joint surgery on patients with osteoarthritis in NW Poland. We found significantly higher concentrations of V and Cr in spongy bone in patients who consumed game meat and also those with prosthetic implants. Chromium levels were significantly lower in patients with kidney diseases. The greatest positive correlations were found between spongy bone V and (i) the amount of consumed beer and (ii) seafood diet. Correlation analysis also showed a significant correlation between Cr levels and seafood diet. To a certain extent these results indicate that the concentrations of V, Cr, and Ca in the human hip joint tissues are connected with occupational exposure, kidney diseases, diet containing game meat, sea food, beer, and the presence of implants. Furthermore, we noted new types of interactions in specific parts of the femoral head. Vanadium may contribute to the lower bone Ca levels, especially in the external parts (cartilage and cortical bone)