Grover's disease in patients with chronic renal failure receiving hemodialysis: clinicopathologic review of 4 cases

In 4 patients undergoing hemodialysis for chronic renal failure, a transient or persistent, papular and keratotic eruption developed on the trunk and arms. Histologic examination disclosed focal acantholysis with dyskeratosis. The lesions were clinically and histologically indistinguishable from those of Grover's disease. A possible association with Grover's disease and chronic renal failure and/or hemodialysis is postulated. Possible implicated pathogenic mechanisms are discussed. We suggest that Grover's disease should be included in the differential diagnosis of cutaneous eruptions in patients with chronic renal failure.     

Oncology research in Saudi Arabia over a 10-year period: A synopsis

Objectives:To assess the quality and quantity of Saudi publications in oncology over a 10-year period.Methods:A systematic PubMed search was conducted between January 2008 and December 2017 to retrieve all Saudi oncology publications. Data about the articles was collected. The level of evidence (LOE) was independently assessed by 2 authors. Two 5-year periods (2008-2012 and 2013-2017) were compared using the relevant parameters. Clinicaltrials.gov was also searched for all oncology trials registered in Saudi Arabia.Results:A total of 839 publications met our inclusion criteria. The most common type of research was case series, totaling 32% of all publications. Clinical trials formed less than 2% of the total. The LOE was I, II, III, and IV in 0.3%, 2.1%, 58.4%, and 39.3% of the included publications, respectively. The LOE was the same in the 2 periods. There were more publications in international journals (p=0.004), more international collaborations (p=0.001), and higher journal impact factors (p=0.037) in 2013-2017 than in 2008-2012. Only 76 registered clinical trials were found in the Clinicaltrials.gov registry.Conclusion:Despite an increase in the number of Saudi publications in the field of oncology over time, the LOE did not change. There were, however, some improvements in the international collaboration and journal impact factor, as well as an increase in the number of studies published in international journals. These observations call for a national strategy to improve oncology research in Saudi Arabia.     

工作环境效能问卷阿拉伯语版的信效度检验

目的 确定工作环境效能问卷-Ⅱ(the Condition for Workplace Effectiveness Questionnaire-Ⅱ,CWEQ-Ⅱ)阿拉伯语版的心理测量学特征,此问卷用于测量护士结构性赋权的现状.为了提高问卷在阿拉伯语国家研究人员中的可用性和可信性,有必要提供有效及可靠的阿拉伯语版本问卷....     

Elevated serum 8-oxo-dG in hemodialysis patients: a marker of systemic inflammation?

Does inflammation, as assessed by high sensitivity C-reactive protein (hs-CRP), in patients with end-stage renal disease (ESRD) tightly associate with increased serum levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8- oxo-dG)? Increased oxidative stress and inflammation have both been highlighted among several nontraditional risk factors for cardiovascular disease, which is the main cause of mortality in ESRD patients. In contrast to oxidative stress effects on proteins and lipids, DNA base damage has not been well demonstrated in ESRD. Two groups of hemodialysis patients were studied, one group with persistent inflammation (n = 13, with constant elevation of CRP > 10 mg/L for 6 months) and one group of noninflamed patients (n = 19, with constant CRP < 10 mg/L for 6 months). Serum 8-oxo-dG was significantly elevated in persistent inflammation in comparison to noninflamed patients. At an individual level, a significant correlation was found between serum 8-oxo-dG and hsCRP. Extracellular 8-oxo-dG leads to intracellular oxidative damage on the nucleotide pool, thus providing a sensitive marker for inflammatory response. Serum levels of 8-oxo-dG, in combination with other inflammatory markers, serve as useful diagnostic tools for identification of patients in risk for inflammatory complications.     

Mitochondrial biogenesis in the pulmonary vasculature during inhalational lung injury and fibrosis

Cell survival and injury repair is facilitated by mitochondrial biogenesis; however, the role of this process in lung repair is unknown. We evaluated mitochondrial biogenesis in the mouse lung in two injuries that cause acute inflammation and in two that cause chronic inflammation and pulmonary fibrosis. By using reporter mice that express green fluorescent protein (GFP) exclusively in mitochondria, we tracked mitochondrial biogenesis and correlated it with histologic lung injury, proliferation, and fibrosis. At 72 hours after acute LPS or continuous exposure to hyperoxia (Fio2, 1.0), the lungs showed diffuse infiltration by inflammatory cells in the alveolar region. In reporter mice, patchy new mitochondrial fluorescence was found in the alveolar region but was most prominent and unexpected in perivascular regions. At 14 days after instillation of asbestos or bleomycin, diffuse chronic inflammation had developed, and green fluorescence appeared in inflammatory cells in the expanded interstitium and was most intense in smooth muscle cells of pulmonary vessels. In all four lung injuries, mitochondrial fluorescence colocalized with mitochondrial superoxide dismutase, but not with proliferating cell nuclear antigen. These data indicate that vascular mitochondrial biogenesis is activated in diverse inhalational lung injuries along with oxidative stress. This finding indicates a unique and unexpected mechanism of metabolic adaptation to pulmonary fibrotic injuries.     

Interleukin-10 (IL-10) secretion in systemic lupus erythematosus and rheumatoid arthritis: IL-10-dependent CD4+CD45RO+ T cell-B cell antibody synthesis

Interleukin-10 (IL-10) is a major immunoregulatory cytokine and has a multitude of immunomodulatory effects in the immune system. In this study, we have examined the secretion andin vitro function of IL-10 in B cell hyperactivity in antibody production in two common autoimmune diseases, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). IL-10 was detectable in serum of all active SLE and serum and synovial fluid samples of all RA patients but in none of the normal controls. B cells and CD4+CD45RO+ memory T cells secreted highly enhanced levels of IL-10 in SLE and RA versus normals. Increased IgM and IgG production by B cells-CD4+CD45RO+ T cells in SLE and RA was IL-10 dependent, since neutralization of IL-10 cytokine by anti-IL-10 antibody drastically reduced Ig synthesis in these coculture experiments. B cell hyperactivity in autoantibody production in SLE and RA may be a function of IL-10-dependent CD4+CD45RO+ Th2 cell activation. Therefore, IL-10 may play an important role in highly disturbed immune system and B cell-T cell function in these immune disorders.     

Increased killer immunoglobulin-like receptor expression and functional defects in natural killer cells in lung cancer

Frequencies of natural killer (NK) cells from patients with non-small cell lung cancer (NSCLC) or small cell lung cancer (SCLC) did not differ from healthy controls. A higher proportion of NK cells from NSCLC patients expressed the killer immunoglobulin-like receptor (KIR) CD158b than in controls (P = 0.0004), in the presence or absence of its ligand, HLA-C1. A similar result was obtained for CD158e in the presence of its ligand HLA-Bw4 in NSCLC patients (P = 0.003); this was entirely attributable to the Bw4I group of alleles in the presence of which a fivefold higher percentage of CD158e(+) NK cells was found in NSCLC patients than controls. Proportions of CD158b(+) NK cells declined with advancing disease in NSCLC patients. Expression of NKp46, CD25 and perforin A, and production of interferon-γ following stimulation with interleukin-12 and interleukin-18, were all significantly lower in NK cells from NSCLC patients than in controls. Both NK cell cytotoxicity and granzyme B expression were also reduced in lung cancer patients. Increased inhibitory KIR expression would decrease NK cell cytotoxic function against tumour cells retaining class I HLA expression. Furthermore, the reduced ability to produce interferon-γ would restrict the ability of NK cells to stimulate T-cell responses in patients with lung cancer.