Role of bundled intervention in reducing surgical site infection rate in gynecologic surgeries

Background: Surgical site infection (SSI) is most common nosocomial infection (15%) among surgical patient’s and contributes significantly to morbidity and mortality. CDC (2015) provides “bundled intervention for prevention of SSI. The present study was planned to evaluate the feasibility and usefulness of these bundled intervention in reducing SSI in our setup. Objectives of this study to study the effect of bundled interventions on SSI in gynaecologic surgery.Methods: A total 50 cases  undergoing gynecological surgery in elective OT included in pilot group and bundled intervention followed  these pilot group cases compared with 50 control group operated in same OT in which bundled intervention not followed outcome measures recorded were Incidence of SSI, type of SSI, need for antibiotic usage, need for secondary suturing, duration of hospital stay.Results: Out of 50 subjects in pilot group, five developed signs and symptoms of SSI giving an SSI rate of 10%. Out of those five, two had superficial SSI and three had deep SSI, none of the patient had organ space SSI.SSI rate in 50 cases operated in the same operating room during the same time period without use of bundled interventions (control group) was 12%.Conclusions: Bundled approach is easy and feasible in all setups. It adds only three extra minutes to the total duration of the surgery with risk reduction of SSI

REST-mediated recruitment of polycomb repressor complexes in mammalian cells.

Polycomb Repressive Complex (PRC) 1 and PRC2 regulate genes involved in differentiation and development. However, the mechanism for how PRC1 and PRC2 are recruited to genes in mammalian cells is unclear. Here we present evidence for an interaction between the transcription factor REST, PRC1, and PRC2 and show that RNF2 and REST co-regulate a number of neuronal genes in human teratocarcinoma cells (NT2-D1). Using NT2-D1 cells as a model of neuronal differentiation, we furthermore showed that retinoic-acid stimulation led to displacement of PRC1 at REST binding sites, reduced H3K27Me3, and increased gene expression. Genome-wide analysis of Polycomb binding in Rest⁻/⁻ and Eed⁻/⁻ mouse embryonic stem (mES) cells showed that Rest was required for PRC1 recruitment to a subset of Polycomb regulated neuronal genes. Furthermore, we found that PRC1 can be recruited to Rest binding sites independently of CpG islands and the H3K27Me3 mark. Surprisingly, PRC2 was frequently increased around Rest binding sites located in CpG-rich regions in the Rest⁻/⁻ mES cells, indicating a more complex interplay where Rest also can limit PRC2 recruitment. Therefore, we propose that Rest has context-dependent functions for PRC1- and PRC2- recruitment, which allows this transcription factor to act both as a recruiter of Polycomb as well as a limiting factor for PRC2 recruitment at CpG islands

A guide to epigenetics in leukaemia stem cells.

Publication status: PublishedLeukaemia stem cells (LSCs) are the critical seed for the growth of haematological malignancies, driving the clonal expansion that enables disease initiation, relapse and often resistance. Specifically, they display inherent phenotypic and epigenetic plasticity resulting in complex heterogenic diseases. In this review, we discuss the key principles of deregulation of epigenetic processes that shape this disease evolution. We consider measures to define and quantify clonal heterogeneity, combining information from recent studies assessing mutational, transcriptional and epigenetic landscapes at single cell resolution in Myeloid Neoplasms (MN). We highlight the importance of integrating epigenetic and genetic information to better understand inter- and intra-patient heterogeneity and discuss how this understanding further informs evolution and progression trajectories and subsequent clinical response in MN. Under this topic, we also discuss efforts to identify mechanisms of resistance, by longitudinal analysis of patient samples. Finally, we highlight how we might target these aberrant epigenetic processes for better therapeutic outcomes and to potentially eradicate LSCs

REST-mediated recruitment of polycomb repressor complexes in mammalian cells.

Polycomb Repressive Complex (PRC) 1 and PRC2 regulate genes involved in differentiation and development. However, the mechanism for how PRC1 and PRC2 are recruited to genes in mammalian cells is unclear. Here we present evidence for an interaction between the transcription factor REST, PRC1, and PRC2 and show that RNF2 and REST co-regulate a number of neuronal genes in human teratocarcinoma cells (NT2-D1). Using NT2-D1 cells as a model of neuronal differentiation, we furthermore showed that retinoic-acid stimulation led to displacement of PRC1 at REST binding sites, reduced H3K27Me3, and increased gene expression. Genome-wide analysis of Polycomb binding in Rest⁻/⁻ and Eed⁻/⁻ mouse embryonic stem (mES) cells showed that Rest was required for PRC1 recruitment to a subset of Polycomb regulated neuronal genes. Furthermore, we found that PRC1 can be recruited to Rest binding sites independently of CpG islands and the H3K27Me3 mark. Surprisingly, PRC2 was frequently increased around Rest binding sites located in CpG-rich regions in the Rest⁻/⁻ mES cells, indicating a more complex interplay where Rest also can limit PRC2 recruitment. Therefore, we propose that Rest has context-dependent functions for PRC1- and PRC2- recruitment, which allows this transcription factor to act both as a recruiter of Polycomb as well as a limiting factor for PRC2 recruitment at CpG islands

Mercury and Other Biomedical Waste Management Practices among Dental Practitioners in India

Objectives. The objective of the study was to assess the awareness and performance towards dental waste including mercury management policy and practices among the dental practitioners in North India. Materials and Methods. An epidemiologic survey was conducted among 200 private dental practitioners. The survey form was composed of 29 self-administered questions frame based on knowledge, attitude, and those regarding the practices of dentists in relation to dental health-care waste management. The resulting data were coded and a statistical analysis was done. Results and Discussion. About 63.7% of the dentists were not aware of the different categories of biomedical waste generated in their clinics. Only 31.9% of the dentists correctly said that outdated and contaminated drugs come under cytotoxic waste. 46.2% said they break the needle and dispose of it and only 21.9% use needle burner to destroy it. 45.0% of the dentists dispose of the developer and fixer solutions by letting them into the sewer, 49.4% of them dilute the solutions and let them into sewer and only 5.6% return them to the supplier. About 40.6% of the dentists dispose of excess silver amalgam by throwing it into common bin. Conclusion. It was concluded that not all dentists were aware of the risks they were exposed to and only half of them observe infection control practices

Accidental phosgene gas exposure: A review with background study of 10 cases

Here, authors present a review on clinical presentation and management of exposure of phosgene gas after reviewing the literature by searching with keywords phosgene exposure on Google, Cochrane, Embase and PubMed with a background of experience gained from 10 patients who were admitted to our institute after an accidental phosgene exposure in February 2011 nearby a city in India. Phosgene is a highly toxic gas, occupational workers may have accidental exposure. The gas can also be generated inadvertently during fire involving plastics and other chemicals and solvents containing chlorine, which is of concern to emergency responders. Phosgene inhalation may cause initially symptoms of respiratory tract irritation, patients feel fine thereafter, and then die of choking a day later because of build up of fluid in the lungs (delayed onset non-cardiogenic pulmonary edema). Phosgene exposure is associated with significant morbidity and mortality. Patients with a history of exposure should be admitted to the hospital for a minimum of 24 h for observation because of the potential for delayed onset respiratory failure and acute respiratory distress syndrome

Structural and ion transport studies on polymer electrolyte [polyvinyl alcohol : 1-ethyl, 3-methyl imadazolium tosylate (IL)] system

177-182In the present work, improvement in ion transport property of polyvinyl alcohol (PVA)-based polymer electrolytes have been investigated. The polymer electrolytes (PEs) systems were prepared by solution cast technique. This PE was subsequently characterized by XRD, IR, optical and electrical measurement. The structural characterizations of electrolytes were investigated under the XRD, IR and optical studies. The bulk electrical of 50 PVA: 50 IL electrolyte system has been found to be 1.34 10-4 S/cm. </span

Histone deacetylase 4 promotes type I interferon signaling, restricts DNA viruses, and is degraded via vaccinia virus protein C6.

Interferons (IFNs) represent an important host defense against viruses. Type I IFNs induce JAK-STAT signaling and expression of IFN-stimulated genes (ISGs), which mediate antiviral activity. Histone deacetylases (HDACs) perform multiple functions in regulating gene expression and some class I HDACs and the class IV HDAC, HDAC11, influence type I IFN signaling. Here, HDAC4, a class II HDAC, is shown to promote type I IFN signaling and coprecipitate with STAT2. Pharmacological inhibition of class II HDAC activity, or knockout of HDAC4 from HEK-293T and HeLa cells, caused a defective response to IFN-α. This defect in HDAC4-/- cells was rescued by reintroduction of HDAC4 or catalytically inactive HDAC4, but not HDAC1 or HDAC5. ChIP analysis showed HDAC4 was recruited to ISG promoters following IFN stimulation and was needed for binding of STAT2 to these promoters. The biological importance of HDAC4 as a virus restriction factor was illustrated by the observations that (i) the replication and spread of vaccinia virus (VACV) and herpes simplex virus type 1 (HSV-1) were enhanced in HDAC4-/- cells and inhibited by overexpression of HDAC4; and (ii) HDAC4 is targeted for proteasomal degradation during VACV infection by VACV protein C6, a multifunctional IFN antagonist that coprecipitates with HDAC4 and is necessary and sufficient for HDAC4 degradation.This work was supported by the Wellcome Trust. GLS is a Wellcome Trust Principal Research Fellow. Yongxu Lu, Andrei I. Smid, Jennifer H. Stuart and Liane Dupont were supported by the Wellcome Trust, Joseph S. Snowden was supported by the Lister Institute and Callum Talbot-Cooper was supported by the BBSRC