Sulfur-induced c(4×4) reconstruction of the Si(001) surface studied by scanning tunneling microscopy

Scanning tunneling microscopy and low-energy electron diffraction have been used to study the adsorption and subsequent thermal desorption of molecular sulfur from the Si(001) surface. Room-temperature adsorption of sulfur resulted in the formation of an overlayer, displaying a high density of vacancies or defects, with the underlying Si(001) surface retaining the (2×1) reconstruction. Annealing this surface to 325 °C leads to the desorption of the sulfur overlayer and the appearance of coexisting c(4×4) and (2×1) surface reconstructions. Our data suggest that the c(4×4) reconstruction is an adsorbate-induced structure in which the sulfur creates defects during the desorption process. High-resolution filled- and empty-state images of the c(4×4) surface lead us to propose a missing-dimer defect model for this reconstruction

Veteran experiences of living with chronic pain in the context of VA care and an opioid 'epidemic'

While chronic pain is an increasingly prevalent condition in the United States, it is twice as common among the military veteran population. As many Vietnam War era veterans are aging and experiencing comorbid medical conditions, their chronic pain is becoming increasingly complex. Policies enacted in response to the ‘opioid epidemic’ have in some ways made treatment of pain safer, but have also left remaining questions regarding how to properly provide care. There are three fields of complexity that interact within this topic: patients with a clear need for care and pain management, providers committed to helping patients, and structural barriers that unintentionally interfere with the provision of care. The lived experience of chronic pain and receiving care through the VA healthcare system combined with a common military culture exemplifies a lifeworld centered on pain—which I call a ‘painworld.’ This painworld is seen in the illness narratives of older, white, male veterans with chronic pain. Examining the way a single VA site provides pain care shows the providers are dedicated to treating veteran patients and offer a large number of treatment options. While the need for pain management services is clear from both the patient and provider perspectives, translating the lived experience of these veterans and their medical needs into a hierarchical bureaucratic structure is difficult. Furthermore, the bureaucratic nature of a large federal organization creates gaps in the healthcare system. This leads to the creation of informal systems through systems-correcting praxis to fill the gaps and attempt to prevent siloing and slippage throughout. Together, these fields of complexity are organized into three chapters, building the argument that the convergence of veteran painworlds, pain care, and bureaucracy can contribute to miscommunication, leading to unintended slippage through the system and inadequate care, despite good intentions of staff. Furthermore, the VA system and structure of providing pain care both influences and is part of the painworld, as are the interactions that occur between veteran patients and staff

Labelled StealthR liposomes in experimental infection : an alternative to leukocyte scintigraphy?

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Role of Interleukin 17 in arthritis chronicity through survival of synoviocytes via regulation of synoviolin expression

Background: The use of TNF inhibitors has been a major progress in the treatment of chronic inflammation. However, not all patients respond. In addition, response will be often lost when treatment is stopped. These clinical aspects indicate that other cytokines might be involved and we focus here on the role of IL-17. In addition, the chronic nature of joint inflammation may contribute to reduced response and enhanced chronicity. Therefore we studied the capacity of IL-17 to regulate synoviolin, an E3 ubiquitin ligase implicated in synovial hyperplasia in human rheumatoid arthritis (RA) FLS and in chronic reactivated streptococcal cell wall (SCW)-induced arthritis.<p></p> Methodology/Principal Findings: Chronic reactivated SCW-induced arthritis was examined in IL-17R deficient and wild-type mice. Synoviolin expression was analysed by real-time RT-PCR, Western Blot or immunostaining in RA FLS and tissue, and p53 assessed by Western Blot. Apoptosis was detected by annexin V/propidium iodide staining, SS DNA apoptosis ELISA kit or TUNEL staining and proliferation by PCNA staining. IL-17 receptor A (IL-17RA), IL-17 receptor C (IL-17-RC) or synoviolin inhibition were achieved by small interfering RNA (siRNA) or neutralizing antibodies. IL-17 induced sustained synoviolin expression in RA FLS. Sodium nitroprusside (SNP)-induced RA FLS apoptosis was associated with reduced synoviolin expression and was rescued by IL-17 treatment with a corresponding increase in synoviolin expression. IL-17RC or IL-17RA RNA interference increased SNP-induced apoptosis, and decreased IL-17-induced synoviolin. IL-17 rescued RA FLS from apoptosis induced by synoviolin knockdown. IL-17 and TNF had additive effects on synoviolin expression and protection against apoptosis induced by synoviolin knowndown. In IL-17R deficient mice, a decrease in arthritis severity was characterized by increased synovial apoptosis, reduced proliferation and a marked reduction in synoviolin expression. A distinct absence of synoviolin expressing germinal centres in IL-17R deficient mice contrasted with synoviolin positive B cells and Th17 cells in synovial germinal centre-like structures.<p></p> Conclusion/Significance: IL-17 induction of synoviolin may contribute at least in part to RA chronicity by prolonging the survival of RA FLS and immune cells in germinal centre reactions. These results extend the role of IL-17 to synovial hyperplasia.<p></p&gt

Detecting infection and inflammation with technetium-99m-labeled stealth liposomes

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