1,162 research outputs found

    Risk Factors Analysis of Surgical Infection Using Artificial Intelligence: A Single Center Study

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    Background: Surgical site infections (SSIs) have a major role in the evolution of medical care. Despite centuries of medical progress, the management of surgical infection remains a pressing concern. Nowadays, the SSIs continue to be an important factor able to increase the hospitalization duration, cost, and risk of death, in fact, the SSIs are a leading cause of morbidity and mortality in modern health care. Methods: A study based on statistical test and logistic regression for unveiling the association between SSIs and different risk factors was carried out. Successively, a predictive analysis of SSIs on the basis of risk factors was performed. Results: The obtained data demonstrated that the level of surgery contamination impacts significantly on the infection rate. In addition, data also reveals that the length of postoperative hospital stay increases the rate of surgical infections. Finally, the postoperative length of stay, surgery department and the antibiotic prophylaxis with 2 or more antibiotics are a significant predictor for the development of infection. Conclusions: The data report that the type of surgery department and antibiotic prophylaxis there are a statistically significant predictor of SSIs. Moreover, KNN model better handle the imbalanced dataset (48 infected and 3983 healthy), observing highest accuracy value

    Pathophysiological mechanisms in neurodevelopmental disorders caused by rac GTPases dysregulation: What’s behind neuro-RACopathies

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    Rho family guanosine triphosphatases (GTPases) regulate cellular signaling and cytoskele-tal dynamics, playing a pivotal role in cell adhesion, migration, and cell cycle progression. The Rac subfamily of Rho GTPases consists of three highly homologous proteins, Rac 1–3. The proper function of Rac1 and Rac3, and their correct interaction with guanine nucleotide-exchange factors (GEFs) and GTPase-activating proteins (GAPs) are crucial for neural development. Pathogenic variants affecting these delicate biological processes are implicated in different medical conditions in humans, primarily neurodevelopmental disorders (NDDs). In addition to a direct deleterious effect produced by genetic variants in the RAC genes, a dysregulated GTPase activity resulting from an abnormal function of GEFs and GAPs has been involved in the pathogenesis of distinctive emerging conditions. In this study, we reviewed the current pertinent literature on Rac-related disorders with a primary neurological involvement, providing an overview of the current knowledge on the pathophysiological mechanisms involved in the neuro-RACopathies

    Regulation of NFKB through the nuclear processing of p105 (NFKB1) in Epstein-Barr Virus immortalized B cell lines.

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    Transcription factors of the NF-κB/Rel family are retained in the cytoplasm as inactive complexes through association with IκB inhibitory proteins. Several NF-κB activators induce the proteolysis of IκB proteins, which results in the nuclear translocation and DNA binding of NF-κB complexes. Here, we report a novel mechanism of NF-κB regulation mediated by p105 (NF-κB1) precursor of p50 directly at the nuclear level. In Epstein- Barr virus-immortalized B cells, p105 was found in the nucleus, where it was complexed with p65. In concomitance with NF-κB activation, mitomycin C induced the processing of p105 to p50 in the nucleus, while it did not affect the steady-state protein levels of IκBα and p105 in the cytoplasm. Differently, phorbol 12-myristate 13-acetate induced a significant proteolysis of both IκBα and p105 in the cytoplasm, while it did not affect the protein level of p105 in the nucleus. These results suggest that in Epstein-Barr virus-positive B cell lines the nuclear processing of p105 can contribute to NF-κB activation in response to specific signaling molecules, such as DNA-damaging agents

    Impairment of methyl cycle affects mitochondrial methyl availability and glutathione level in Down's Sindrome

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    In Down's syndrome there is evidence that increased gene expression coding for specific cystathionine beta-synthase translates directly into biochemical aberrations, which result in a biochemical and metabolic imbalance of the methyl status. This event is destined to impact mitochondrial function since methylation is a necessary event in mitochondria and relies on the availability and uptake of the methyl donor S-adenosylmethionine. Indeed mitochondrial dysfunctions have been widely described in Down's syndrome, but they have never been correlated to a possible mitochondrial methyl unbalance. In the present study we find that the mitochondrial levels of S-adenosylmethionine are reduced in Down's syndrome compared to control cells demonstrating the effect of the methyl unbalance on mitochondria. The possible role of methylation in mitochondria is discussed and some preliminary results on a possible methylation target are presented

    Non-Markovian dynamics of interacting qubit pair coupled to two independent bosonic baths

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    The dynamics of two interacting spins coupled to separate bosonic baths is studied. An analytical solution in Born approximation for arbitrary spectral density functions of the bosonic environments is found. It is shown that in the non-Markovian cases concurrence "lives" longer or reaches greater values.Comment: 13 page

    Impairment of methyl cycle affects mitochondrial methyl availability and glutathione level in Down's Sindrome

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    In Down's syndrome there is evidence that increased gene expression coding for specific cystathionine beta-synthase translates directly into biochemical aberrations, which result in a biochemical and metabolic imbalance of the methyl status. This event is destined to impact mitochondrial function since methylation is a necessary event in mitochondria and relies on the availability and uptake of the methyl donor S-adenosylmethionine. Indeed mitochondrial dysfunctions have been widely described in Down's syndrome, but they have never been correlated to a possible mitochondrial methyl unbalance. In the present study we find that the mitochondrial levels of S-adenosylmethionine are reduced in Down's syndrome compared to control cells demonstrating the effect of the methyl unbalance on mitochondria. The possible role of methylation in mitochondria is discussed and some preliminary results on a possible methylation target are presented

    Dynamic identification of a strategic building of the sixties with a mixed structure

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    The present paper shows and discusses the results of the identification procedure applied to the building of the Municipality of Castellaneta, Taranto (Puglia, Italy). The case study has been chosen for its structural complexity; indeed, the building has been built in two successive phases, block A built between 1955 and 1957, and block B, for completion, presumably built between the years 1960 and 1961. Block A constitutes the main building and represents the original nucleus. The structure was subsequently subject to structural interventions to replace some load-bearing walls with steel beams. The building constituting block B, joined to the original body of the building, has a structure in load-bearing masonry, while the floors, more recently built, are also in brick-concrete, but with pre-cast prestressed joists. The dynamic response of the building was assessed through OMA (Operational Modal Analysis) identification technique which allows you to determine the properties of the structure in real operating conditions, without the need to interrupt the activities inside the structure itself. The structural excitement, therefore, is due only to the environmental condition. A 3D model was defined in PRO_SAP; the results obtained from the finite element model were subsequently compared with those obtained from the experimental model

    Chronic low back pain patients' use of, level of knowledge of and perceived benefits of complementary medicine: a cross-sectional study at an academic pain center.

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    Chronic pain patients often use complementary medicine (CM) to alleviate their pain; however, little is known about the use of CM by chronic low back pain (cLBP) patients. We investigated the frequency of use of CM by cLBP patients, the perceived effects of these therapies, patients' knowledge regarding CM, and patient-physician communication regarding CM. A cross-sectional survey was conducted from November 2014 to February 2015. A questionnaire was distributed by physicians to 238 consecutive patients consulting for cLBP at the Pain Center of Lausanne University Hospital, Switzerland. Poisson regression model was used to analyze patients' level of knowledge regarding various CMs, and the logistic regression model was used to assess CM use for cLBP. The questionnaire was returned by 168 cLBP patients (response rate: 70.6%). Lifetime prevalence of CM use for cLBP was 77.3%. The most commonly used therapies were osteopathy (48.8%), massage (45.2%) and acupuncture (31.6%), rated for their usefulness on a 0-10 scale as a mean ± SD of 5.4 ± 2.7, 5.9 ± 2.5 and 3.8 ± 3.2, respectively. The CM treatment best known by patients was osteopathy, followed by massage and acupuncture. If their doctors proposed CM as a treatment for cLBP, 78% of participants reported being very or somewhat likely to try CM. Respondents with CM health insurance were more likely to use CM (OR = 2.26; 95%CI: 1.07-4.78; p = 0.031) for cLBP. Respondents having experienced cLBP for more than five years were more likely to use CM to treat their cLBP than respondents having experienced cLBP for one year or less (OR = 2.84; 95%CI: 1.02-7.88; p = 0.044). More than three-quarters of cLBP patients in our sample did use CM to treat their cLBP. The results showed that the most commonly used therapies were not necessarily the highest rated in terms of perceived usefulness. These results highlight the importance of developing integrative pain centers in which patients may obtain advice regarding CM treatments

    Partial purification and MALDI-TOF MS analysis of UN1, a tumor antigen membrane glycoprotein.

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    UN1 is a membrane glycoprotein that is expressed in immature human thymocytes, a subpopulation of peripheral T lymphocytes, the HPB acute lymphoblastic leukemia (ALL) T-cell line and fetal thymus. We previously reported the isolation of a monoclonal antibody (UN1 mAb) recognizing the UN1 protein that was classified as "unclustered" at the 5th and 6th International Workshop and Conference on Human Leukocyte Differentiation Antigens. UN1 was highly expressed in breast cancer tissues and was undetected in non-proliferative lesions and in normal breast tissues, indicating a role for UN1 in the development of a tumorigenic phenotype of breast cancer cells. In this study, we report a partial purification of the UN1 protein from HPB-ALL T cells by anion-exchange chromatography followed by immunoprecipitation with the UN1 mAb and MALDI-TOF MS analysis. This analysis should assist in identifying the amino acid sequence of UN
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