Bacillus Cereus Catheter Related Bloodstream Infection in a Patient with Acute Lymphoblastic Leukemia

Bacillus cereus infection is rarely associated with actual infection and for this reason single positive blood culture is usually regarded as contamination . However it may cause a number of infections, such catheter-related bloodstream infections. Significant catheter-related bloodstream infections (CRBSI) caused by Bacillus spp. are mainly due to B. cereus and have been predominantly reported in immunocompromised hosts. Catheter removal is generally advised for management of infection. In this report, catheter-related bacteremia caused by B. cereus in a patient with acute lymphoblast c leukemia (ALL) in Istanbul Medical Faculty was presented

Cockayne syndrome group B protein has novel strand annealing and exchange activities

Cockayne syndrome (CS) is a rare inherited human genetic disorder characterized by UV sensitivity, severe neurological abnormalities and prageroid symptoms. The CS complementation group B (CSB) protein is involved in UV-induced transcription coupled repair (TCR), base excision repair and general transcription. CSB also has a DNA-dependent ATPase activity that may play a role in remodeling chromatin in vivo. This study reports the novel finding that CSB catalyzes the annealing of complementary single-stranded DNA (ssDNA) molecules with high efficiency, and has strand exchange activity. The rate of CSB-catalyzed annealing of complementary ssDNA is 25-fold faster than the rate of spontaneous ssDNA annealing under identical in vitro conditions and the reaction occurs with a high specificity in the presence of excess non-homologous ssDNA. The specificity and intrinsic nature of the reaction is also confirmed by the observation that it is stimulated by dephosphorylation of CSB, which occurs after UV-induced DNA damage, and is inhibited in the presence of ATPγS. Potential roles of CSB in cooperation with strand annealing and exchange activities for TCR and homologous recombination are discussed

Cockayne syndrome B protein stimulates apurinic endonuclease 1 activity and protects against agents that introduce base excision repair intermediates

The Cockayne syndrome B (CSB) protein—defective in a majority of patients suffering from the rare autosomal disorder CS—is a member of the SWI2/SNF2 family with roles in DNA repair and transcription. We demonstrate herein that purified recombinant CSB and the major human apurinic/apyrimidinic (AP) endonuclease, APE1, physically and functionally interact. CSB stimulates the AP site incision activity of APE1 on normal (i.e. fully paired) and bubble AP–DNA substrates, with the latter being more pronounced (up to 6-fold). This activation is ATP-independent, and specific for the human CSB and full-length APE1 protein, as no CSB-dependent stimulation was observed with Escherichia coli endonuclease IV or an N-terminal truncated APE1 fragment. CSB and APE1 were also found in a common protein complex in human cell extracts, and recombinant CSB, when added back to CSB-deficient whole cell extracts, resulted in increased total AP site incision capacity. Moreover, human fibroblasts defective in CSB were found to be hypersensitive to both methyl methanesulfonate (MMS) and 5-hydroxymethyl-2′-deoxyuridine, agents that introduce base excision repair (BER) DNA substrates/intermediates

Evidence for B cell exhaustion in chronic graft-versus-host disease

Chronic graft-versus-host disease (cGvHD) remains a major complication of allogeneic hematopoietic stem cell transplantation (HSCT). A number of studies support a role for B cells in the pathogenesis of cGvHD. In this study, we report the presence of an expanded population of CD19+CD21− B cells with features of exhaustion in the peripheral blood of patients with cGvHD. CD21− B cells were significantly increased in patients with active cGvHD compared to patients without cGvHD and healthy controls (median 12.2 versus 2.12 versus 3%, respectively; p < 0.01). Compared with naïve (CD27−CD21+) and classical memory (CD27+CD21+) B cells, CD19+CD21− B cells in cGvHD were CD10 negative, CD27 negative and CD20hi, and exhibited features of exhaustion, including increased expression of multiple inhibitory receptors such as FCRL4, CD22, CD85J, and altered expression of chemokine and adhesion molecules such as CD11c, CXCR3, CCR7, and CD62L. Moreover, CD21− B cells in cGvHD patients were functionally exhausted and displayed poor proliferative response and calcium mobilization in response to B-cell receptor triggering and CD40 ligation. Finally, the frequencies of circulating CD21− B cells correlated with cGvHD severity in patients after HSCT. Our study further characterizes B cells in chronic cGVHD and supports the use of CD21−CD27−CD10− B cell frequencies as a biomarker of disease severity

Asymptomatic giant coronary aneurysm in an adolescent with Behcet's syndrome

<p>Abstract</p> <p>Objective</p> <p>Behcet's is an idiopathic multi-organ syndrome, which may have onset during childhood. Vascular involvement is uncommon, with rarely reported coronary aneurysm formation. We present a case report of a teenager girl who developed recalcitrant life-threatening Behcet's vasculitis, involving both small and large venous and arterial systems including a giant coronary aneurysm.</p> <p>Case report</p> <p>De-identified data were collected retrospectively in case report format. Although our sixteen year old female with Behcet's vasculitis had resolution of many arterial aneurysms, she had persistent venous thrombosis of large vessels, as well as persistent, giant arterial aneurysms requiring intra-arterial coiling of a lumbar artery and coronary bypass grafting despite intensive immunosuppression including glucocorticoids, cyclophosphamide, infliximab, methotrexate, azathioprine and intravenous immunoglobulin.</p> <p>Conclusions</p> <p>Vascular manifestations may be seen in Behcet's syndrome, including asymptomatic coronary aneurysm, which may be refractory to immunosuppression and ultimately require surgical intervention. Increased awareness is essential for prompt diagnosis and management.</p

Federal Institutions and Strategic Policy Responses to COVID-19 Pandemic

This is the final version. Available on open access from Frontiers Media via the DOI in this recordData Availability Statement: The original contributions presented in the study are included in the article/Supplementary Material; further inquiries can be directed to the corresponding author.This essay examines the policy response of the federal and regional governments in federations to the COVID-19 crisis. We theorize that the COVID-19 policy response in federations is an outcome of strategic interaction among the federal and regional incumbents in the shadow of their varying accountability for health and the repercussions from the disruptive consequences of public health measures. Using the data from the COVID-19 Public Health Protective Policy Index Project, we study how the variables suggested by our theory correlate with the overall stringency of public health measures in federations as well as the contribution of the federal government to the making of these policies. Our results suggest that the public health measures taken in federations are at least as stringent as those in non-federations, and there is a cluster of federations on which a bulk of crisis policy making is carried by subnational governments. We find that the contribution of the federal government is, on average, higher in parliamentary systems; it appears to decline with the proximity of the next election in presidential republics, and to increase with the fragmentation of the legislative party system in parliamentary systems. Our analysis also suggests that when the federal government carries a significant share of responsibility for healthcare provision, it also tends to play a higher role in taking non-medical steps in response to the pandemic

Institutional Origins of Protective COVID-19 Public Health Policy Responses: Informational and Authority Redundancies and Policy Stringency

This is the author accepted manuscript. The final version is available from Now Publishers via the DOI in this recordIn this essay, we argue that institutional systems that allow redundancies in information channels and in policy-making are more likely to generate a rapid policy response to crises such as the onset of COVID-19 pandemic than more streamlined systems. Since democracies and decentralized polities feature higher informational and authority redundancies, we theorize improved crisis response in democracies, and in more decentralized democracies. To assess our theoretical expectations, we construct an original data set of stringency of policy measures that were adopted in response to COVID-19 by governments at different levels in 64~countries between January and May 2020. We find that democracies and liberal democracies responded to COVID-19 stronger and faster. Federalism and decentralization in addition to democratic institutions played a less uniform, but still a positive role. Beyond their other acknowledged merits, democratic institutions have superior capacity to mount a quick policy response to unqualified threats

COVID-19 Policy Response and the Rise of the Sub-National Governments

This is the author accepted manuscript. The final version is available from University of Toronto Press via the DOI in this recordData availability: The data used in this article are available as online Appendices C–G.We examine the roles of sub-national and national governments in Canada and the United States vis-à-vis the protective public health response in the onset phase of the global coronavirus disease 2019 (COVID-19) pandemic. This period was characterized in both countries by incomplete information as well as by uncertainty regarding which level of government should be responsible for which policies. The crisis represents an opportunity to study how national and sub-national governments respond to such policy challenges. In this article, we present a unique dataset that catalogues the policy responses of US states and Canadian provinces as well as those of the respective federal governments: the Protective Policy Index (PPI). We then compare the United States and Canada along several dimensions, including the absolute values of subnational levels of the index relative to the total protections enjoyed by citizens, the relationship between early threat (as measured by the mortality rate near the start of the public health crisis) and the evolution of the PPI, and finally the institutional and legislative origins of the protective health policies. We find that the sub-national contribution to policy is more important for both the United States and Canada than are their national-level policies, and it is unrelated in scope to our early threat measure. We also show that the institutional origin of the policies as evidenced by the COVID-19 response differs greatly between the two countries and has implications for the evolution of federalism in each