Constructing Homeomorphisms Of The Cantor Ternary Set

In this paper, we present a generalized form of the Cantor ternary set by studying the cantor    middle set where 1    and its fractal dimension. The paper also introduces the Heine-Borel set and shows that the cantor set and its generalised   middle set where 1   are Heine-Borel sets

Near-threshold electron transfer in anion-nucleobase clusters : Does the identity of the anion matter?

Laser dissociation spectroscopy of I − ·adenine (I − ·A) and H 2 PO − 3 ·adenine (H 2 PO − 3 ·A) has been utilised for the first time to explore how the anion identity impacts on the excited states. Despite strong photodepletion, ionic photofragmentation is weak for both clusters, revealing that they decay predominantly by electron detachment. The spectra of I − ·A display a prominent dipole-bound excited state in the region of the detachment energy which relaxes to produce deprotonated adenine. In contrast, near-threshold photoexcitation of H 2 PO − 3 ·A does not access a dipole-bound state, but instead displays photofragmentation properties associated with ultrafast decay of an adenine-localised π→π* transition. Notably, the experimental electron detachment onset of H 2 PO − 3 ·A is around 4.7 eV, which is substantially lower than the expected detachment energy of an ion-dipole complex. The low value for H 2 PO − 3 ·A can be traced to initial ionisation of the adenine followed by significant geometric rearrangement on the neutral surface. We conclude that these dynamics quench access to a dipole-bound excited state for H 2 PO − 3 ·A and subsequent electron transfer. H 2 PO − 3 ·A represents an important new example of an ionic cluster where ionisation occurs from the neutral cluster component and where photodetachment initiates intra-molecular hydrogen atom transfer

KLIC-score for predicting early failure in prosthetic joint infections treated with debridement, implant retention and antibiotics

AbstractDebridement, irrigation and antibiotic treatment form the current approach in early prosthetic joint infection (PJI). Our aim was to design a score to predict patients with a higher risk of failure. From 1999 to 2014 early PJIs were prospectively collected and retrospectively reviewed. The primary end-point was early failure defined as: 1) the need for unscheduled surgery, 2) death-related infection within the first 60 days after debridement or 3) the need for suppressive antibiotic treatment. A score was built-up according to the logistic regression coefficients of variables available before debridement. A total of 222 patients met the inclusion criteria. The most frequently isolated microorganisms were coagulase-negative staphylococci (95 cases, 42.8%) and Staphylococcus aureus (81 cases, 36.5%). Treatment of 52 (23.4%) cases failed. Independent predictors of failure were: chronic renal failure (OR 5.92, 95% CI 1.47–23.85), liver cirrhosis (OR 4.46, 95% CI 1.15–17.24), revision surgery (OR 4.34, 95% CI 1.34–14.04) or femoral neck fracture (OR 4.39, 95% CI1.16–16.62) compared with primary arthroplasty, C reactive protein >11.5 mg/dL (OR 12.308, 95% CI 4.56–33.19), cemented prosthesis (OR 8.71, 95% CI 1.95–38.97) and when all intraoperative cultures were positive (OR 6.30, 95% CI 1.84–21.53). A score for predicting the risk of failure was designed using preoperative factors (KLIC-score: Kidney, Liver, Index surgery, Cemented prosthesis and C-reactive protein value) and it ranged between 0 and 9.5 points. Patients with scores of ≤2, >2–3.5, 4–5, >5–6.5 and ≥7 had failure rates of 4.5%, 19.4%, 55%, 71.4% and 100%, respectively. The KLIC-score was highly predictive of early failure after debridement. In the future, it would be necessary to validate our score using cohorts from other institutions

Genomic stability, anti-inflammatory phenotype, and up-regulation of the RNAseH2 in cells from centenarians

Current literature agrees on the notion that efficient DNA repair favors longevity across evolution. The DNA damage response machinery activates inflammation and type I interferon signaling. Both pathways play an acknowledged role in the pathogenesis of a variety of age-related diseases and are expected to be detrimental for human longevity. Here, we report on the anti-inflammatory molecular make-up of centenarian's fibroblasts (low levels of IL-6, type 1 interferon beta, and pro-inflammatory microRNAs), which is coupled with low level of DNA damage (measured by comet assay and histone-2AX activation) and preserved telomere length. In the same cells, high levels of the RNAseH2C enzyme subunit and low amounts of RNAseH2 substrates, i.e. cytoplasmic RNA:DNA hybrids are present. Moreover, RNAseH2C locus is hypo-methylated and RNAseH2C knock-down up-regulates IL-6 and type 1 interferon beta in centenarian's fibroblasts. Interestingly, RNAseH2C locus is hyper-methylated in vitro senescent cells and in tissues from atherosclerotic plaques and breast tumors. Finally, extracellular vesicles from centenarian's cells up-regulate RNAseH2C expression and dampen the pro-inflammatory phenotype of fibroblasts, myeloid, and cancer cells. These data suggest that centenarians are endowed with restrained DNA damage-induced inflammatory response, that may facilitate their escape from the deleterious effects of age-related chronic inflammation