Comparison of bloodstream and non-bloodstream infections caused by carbapenem-resistant Klebsiella pneumoniae in the intensive care unit: a 9-year respective study

BackgroundBloodstream infections (BSIs) caused by carbapenem-resistant Klebsiella pneumoniae (CRKP) have received much attention. However, few studies have identified risk factors for CRKP BSIs in comparison to CRKP non-bloodstream infections (non-BSIs). This study aimed to compare the epidemiology, risk factors, and outcomes of CRKP BSIs and CRKP non-BSIs.MethodsWe conducted a retrospective study of patients infected with CRKP in the ICU from January 2012 to December 2020. Clinical characteristics and outcomes were compared between CRKP BSIs and CRKP non-BSIs. Predictors associated with 28-day all-cause mortality in CRKP-infected patients were also evaluated.Results326 patients infected with CRKP were enrolled, including 96 patients with CRKP BSIs and 230 with CRKP non-BSIs. The rates of CRKP BSIs in CRKP infections were generally raised from 2012 (12.50%) to 2020 (45.76%). Multivariate logistic analysis indicated that the use of carbapenems within the prior 90 days was an independent risk factor for CRKP BSIs (p = 0.019). Compared to CRKP non-BSIs, CRKP isolates in the CRKP BSI group were found to be non-susceptible to more tested carbapenems (p = 0.001). Moreover, the CRKP BSI group exhibited a higher mortality rate (p = 0.036). The non-susceptibility of CRKP isolates to more tested carbapenems (p = 0.025), a high SOFA score (p = 0.000), and the use of antifungal drugs within the prior 90 days (p = 0.018) were significant factors for 28-day all-cause mortality in CRKP-infected patients.ConclusionThe proportion of CRKP BSI increased progressively in CRKP-infected patients over 9 years. The use of carbapenems within the prior 90 days was an independent risk factor for the development of CRKP BSIs. The non-susceptibility of CRKP isolates to more tested carbapenems and a higher mortality rate were found in the CRKP BSI group

Comparison of the effects of different percentages of soy protein in the diet on patients with type 2 diabetic nephropathy: systematic reviews and network meta-analysis

BackgroundDietary soy protein (SP) is a potential intervention for protecting the kidneys and improving glucose and lipid metabolism. However, whether this effect is related to the percentage of SP intake remains unclear.ObjectiveThis study aims to review and analyze the results of randomized clinical trials (RCTs) in patients with type 2 diabetic nephropathy (T2DN) who received diets with different percentages of SP.MethodsThe databases: PubMed, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science, China National Knowledge Infrastructure (CNKI), Chinese BioMedical Literature Database (CBM), WanFang, Weipu (VIP), and ClinicalTrials.gov were searched until February 2023, for RCTs on T2DN and SP.ResultsA total of six studies comprising 116 participants were included. The interventions were classified as 0% SP, 35% SP, and 100% SP. To improve serum creatinine (Scr), blood urea nitrogen (BUN), 24-h urine total protein (24hUTP), and glomerular filtration rate (GFR), a 35% SP diet was the most effective, compared to a 0% SP diet, which showed a mean difference of −154.00 (95% confidence interval: −266.69, −41.31) for 24hUTP. Although it had significant benefits for 24hUTP, great heterogeneity was observed. To improve the glycolipid metabolism-related markers such as cholesterol (CHO), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), fasting blood glucose (FPG), and weight, the 35% SP diet demonstrated superior efficacy compared to the 0% SP diet. Specifically, the mean difference for CHO was −0.55 (95% confidence interval: −1.08, −0.03), and for LDL-C, it was −17.71 (95% confidence interval: −39.67, −4.24). The other indicators were not statistically significant. Most studies had concerns regarding the risk of bias.ConclusionThe findings of this study demonstrate that both 35% and 100% SP diets are more effective than a diet with no SP in improving renal function and glucolipid metabolism in patients with T2DN. As a result, a diet incorporating 35% SP may be the optimal choice for individuals with T2DN.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=352638, identifier CRD42022352638

Knowledge and attitudes of healthcare workers in Chinese intensive care units regarding 2009 H1N1 influenza pandemic

<p>Abstract</p> <p>Background</p> <p>To describe the knowledge and attitudes of critical care clinicians during the 2009 H1N1 influenza pandemic.</p> <p>Methods</p> <p>A survey conducted in 21 intensive care units in 17 provinces in China.</p> <p>Results</p> <p>Out of 733 questionnaires distributed, 695 were completed. Three hundred and fifty-six respondents (51.2%) reported their experience of caring for H1N1 patients. Despite the fact that 88.5% of all respondents ultimately finished an H1N1 training program, only 41.9% admitted that they had the knowledge of 2009 H1N1 influenza. A total of 572 respondents (82.3%) expressed willingness to care for H1N1 patients. Independent variables associated with increasing likelihood to care for patients in the logistic regression analysis were physicians or nurses rather than other professionals (odds ratio 4.056 and 3.235, p = 0.002 and 0.007, respectively), knowledge training prior to patient care (odds ratio 1.531, p = 0.044), and the confidence to know how to protect themselves and their patients (odds ratio 2.109, p = 0.001).</p> <p>Conclusion</p> <p>Critical care clinicians reported poor knowledge of H1N1 influenza, even though most finished a relevant knowledge training program. Implementation of appropriate education program might improve compliance to infection control measures, and willingness to work in a pandemic.</p

Administration of Interleukin-35-Conditioned Autologous Tolerogenic Dendritic Cells Prolong Allograft Survival After Heart Transplantation

Background/Aims: IL-35, a powerful suppressor of inflammation and autoimmunity, is primarily secreted by regulatory T cells (Tregs) and can, in turn, promote Treg differentiation. However, the precise effect of IL-35 on dendritic cells (DCs) remains to be clarified. Methods: In this study, we investigated the expression of IL-35 in DCs after stimulation with LPS utilizing enzyme linked immunosorbent assay(ELISA), quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) and western blotting, and the influence of IL-35 on the maturation and function of DCs by mixed lymphocyte reaction assay and flow cytometry. We further examined the regulation of IL-35 in DCs by the microRNA let-7i (let-7i) via transfected with let-7i mimic, inhibitor or suppressor of cytokine signalling 1 (SOCS1) siRNA. IL-35-overexpressing DCs were transfused into BALB/c recipients with C57BL/6 heart transplantations to verify the role of immune tolerance in transplantation. Results: The results showed that IL-35 expression was significantly up-regulated following lipopolysaccharide (LPS)-induced DC maturation. Overexpression of IL-35 suppressed DC maturation, promoted the secretion of anti-inflammatory cytokines, and subsequently affected the balance between Treg and Th17 cells. IL-35 expression in DCs was regulated by let-7i, which targets SOCS1. The transfusion of IL-35-transfected DCs induced Treg generation in mice and prolonged cardiac allograft survival. Conclusion: Our data demonstrated that IL-35 induces tolerogenic DCs which are capable of alleviating allograft rejection. Clinical application of IL-35-treated DCs might be a promising approach for eliciting cardiac allograft immune tolerance

The Long Noncoding RNA MALAT1 Induces Tolerogenic Dendritic Cells and Regulatory T Cells via miR155/Dendritic Cell-Specific Intercellular Adhesion Molecule-3 Grabbing Nonintegrin/IL10 Axis

By shaping T cell immunity, tolerogenic dendritic cells (tDCs) play critical roles in the induction of immune tolerance after transplantation. However, the role of long noncoding RNAs (lncRNAs) in the function and immune tolerance of dendritic cells (DCs) is largely unknown. Here, we found that the lncRNA MALAT1 is upregulated in the infiltrating cells of tolerized mice with cardiac allografts and activated DCs. Functionally, MALAT1 overexpression favored a switch in DCs toward a tolerant phenotype. Mechanistically, ectopic MALAT1 promoted dendritic cell-specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) expression by functioning as an miR155 sponge, which is essential for the tolerogenic maintenance of DCs and the DC-SIGN-positive subset with more potent tolerogenic ability. The adoptive transfer of MALAT1-overexpressing DCs promoted cardiac allograft survival and protected from the development of experimental autoimmune myocarditis, accompanied with increasing antigen-specific regulatory T cells. Therefore, overexpressed MALAT1 induces tDCs and immune tolerance in heart transplantation and autoimmune disease by the miRNA-155/DC-SIGH/IL10 axis. This study highlights that the lncRNA MALAT1 is a novel tolerance regulator in immunity that has important implications in settings in which tDCs are preferred

Therapeutic potential of human umbilical cord mesenchymal stem cells in the treatment of rheumatoid arthritis

Introduction: Rheumatoid arthritis (RA) is a T-cell-mediated systemic autoimmune disease, characterized by synovium inflammation and articular destruction. Bone marrow mesenchymal stem cells (MSCs) could be effective in the treatment of several autoimmune diseases. However, there has been thus far no report on umbilical cord (UC)-MSCs in the treatment of RA. Here, potential immunosuppressive effects of human UC-MSCs in RA were evaluated. Methods: The effects of UC-MSCs on the responses of fibroblast-like synoviocytes (FLSs) and T cells in RA patients were explored. The possible molecular mechanism mediating this immunosuppressive effect of UC-MSCs was explored by addition of inhibitors to indoleamine 2,3-dioxygenase (IDO), Nitric oxide (NO), prostaglandin E2 (PGE2), transforming growth factor beta 1 (TGF-beta 1) and interleukin 10 (IL-10). The therapeutic effects of systemic infusion of human UC-MSCs on collagen-induced arthritis (CIA) in a mouse model were explored. Results: In vitro, UC-MSCs were capable of inhibiting proliferation of FLSs from RA patients, via IL-10, IDO and TGF-beta 1. Furthermore, the invasive behavior and IL-6 secretion of FLSs were also significantly suppressed. On the other hand, UC-MSCs induced hyporesponsiveness of T cells mediated by PGE2, TGF-beta 1 and NO and UC-MSCs could promote the expansion of CD4(+) Foxp3(+) regulatory T cells from RA patients. More importantly, systemic infusion of human UC-MSCs reduced the severity of CIA in a mouse model. Consistently, there were reduced levels of proinflammatory cytokines and chemokines (TNF-alpha, IL-6 and monocyte chemoattractant protein-1) and increased levels of the anti-inflammatory/regulatory cytokine (IL-10) in sera of UC-MSCs treated mice. Moreover, such treatment shifted Th1/Th2 type responses and induced Tregs in CIA. Conclusions: In conclusion, human UC-MSCs suppressed the various inflammatory effects of FLSs and T cells of RA in vitro, and attenuated the development of CIA in vivo, strongly suggesting that UC-MSCs might be a therapeutic strategy in RA. In addition, the immunosuppressive activitiy of UC-MSCs could be prolonged by the participation of Tregs.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000287517000020&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701RheumatologySCI(E)PubMed64ARTICLE6R2101

Performance modulation of a-MnO2 nanowires by crystal facet engineering

Modulation of material physical and chemical properties through selective surface engineering is currently one of the most active research fields, aimed at optimizing functional performance for applications. The activity of exposed crystal planes determines the catalytic, sensory, photocatalytic, and electrochemical behavior of a material. In the research on nanomagnets, it opens up new perspectives in the fields of nanoelectronics, spintronics, and quantum computation. Herein, we demonstrate controllable magnetic modulation of α-MnO 2 nanowires, which displayed surface ferromagnetism or antiferromagnetism, depending on the exposed plane. First-principles density functional theory calculations confirm that both Mn- and O-terminated α-MnO2(1 1 0) surfaces exhibit ferromagnetic ordering. The investigation of surface-controlled magnetic particles will lead to significant progress in our fundamental understanding of functional aspects of magnetism on the nanoscale, facilitating rational design of nanomagnets. Moreover, we approved that the facet engineering pave the way on designing semiconductors possessing unique properties for novel energy applications, owing to that the bandgap and the electronic transport of the semiconductor can be tailored via exposed surface modulations