653 research outputs found
Postpartum Abdominal Binder Use for Pain Management After Vaginal Delivery – A Randomized Controlled Trial
Objective: To investigate the impact of abdominal binder plus usual care versus usual care alone 26 after spontaneous vaginal delivery on pain severity scores. 27 28 Methods: A prospective randomized study was performed, recruiting patients on a Labor and 29 Delivery unit who were anticipating spontaneous vaginal delivery from 2019 to 2022. Patients 30 were randomly assigned to receive an abdominal binder plus usual care or usual care alone 31 within two hours postpartum. Primary outcomes were patient-reported immediate postpartum 32 pain score and average daily pain scores on days 0 and 1 postpartum (using a scale from 0 to 10, 33 and recorded every 2 hours), and location of pain. Secondary outcomes were use of 34 pharmacologic analgesia and non-pharmacologic methods of pain management. 35 36 Results: Fifty patients received an abdominal binder plus usual care and 50 patients received 37 usual care alone for postpartum pain management. Average pain scores immediately postpartum 38 were elevated in the group who received binders, but not statistically significant compared to the 39 group who received usual care (p = 0.05). Average pain scores on days 0 and 1 postpartum were 40 not significantly different between groups. There were no differences between groups in 41 locations of pain and use of pharmacologic analgesia. 42 43 Conclusion: This study showed no evidence for reduced pain or reduced use of pharmacologic 44 pain interventions with use of an abdominal binder plus usual care after spontaneous vaginal 45 delivery, despite previously studied benefits of binders for antepartum pain control after 46 3 caesarean section. Abdominal binder use did not influence the location of pain reported by 47 patients
The p53-targeting human phosphatase hCdc14A interacts with the Cdk1/cyclin B complex and is differentially expressed in human cancers
BACKGROUND: The evolutionary conserved cyclin-dependent kinase phosphatase hCdc14A has been shown to play potential roles in the regulation of mitotic exit and in the centrosome duplication cycle. We have recently shown that hCdc14A also can interact with the tumor suppressor p53 both in vitro and in vivo and specifically dephosphorylates the ser315 site of p53 in vitro. In this study we developed antibodies against hCdc14A to investigate the expression and regulation of hCdc14A in human tissues and cancer cells. RESULTS: We show that hCdc14A is differentially expressed in human tissues and in 75 cancer cell lines examined. Treatments with the histone deacetylase inhibitor TSA, the demethylating agent 5-aza-2'-deoxycytodine or the proteasome inhibitor MG132 significantly induced expression of hCdc14A in cell lines expressing low or undetectable levels of hCdc14A. There was a strong bias for low expression of hCdc14A in cancer cell lines harboring wild-type p53, suggesting that high Cdc14A expression is not compatible with wild-type p53 expression. We present evidence for a role for hCdc14A in the dephosphorylation of the ser315 site of p53 in vivo and that hCdc14A forms a complex with Cdk1/cyclin B during interphase but not during mitosis. CONCLUSION: Our results that hCdc14A is differentially expressed in human cancer cells and that hCdc14A can interact with both p53 and the Cdk1/cyclin B complex may implicate that dysregulation of hCdc14A expression may play a role in carcinogenesis
Cardiac magnetic resonance imaging and gadolinium angiography for neonates and small infants: a 10-year single institutional experience
Molecular targets for rapid identification of Brucella spp
BACKGROUND: Brucella is an intracellular pathogen capable of infecting animals and humans. There are six recognized species of Brucella that differ in their host preference. The genomes of the three Brucella species have been recently sequenced. Comparison of the three revealed over 98% sequence similarity at the protein level and enabled computational identification of common and differentiating genes. We validated these computational predictions and examined the expression patterns of the putative unique and differentiating genes, using genomic and reverse transcription PCR. We then screened a set of differentiating genes against classical Brucella biovars and showed the applicability of these regions in the design of diagnostic tests. RESULTS: We have identified and tested set of molecular targets that are associated in unique patterns with each of the sequenced Brucella spp. A comprehensive comparison was made among the published genome sequences of B. abortus, B. melitensis and B. suis. The comparison confirmed published differences between the three Brucella genomes, and identified subsets of features that were predicted to be of interest in a functional comparison of B. melitensis and B. suis to B. abortus. Differentiating sequence regions from B. abortus, B. melitensis and B. suis were used to develop PCR primers to test for the existence and in vitro transcription of these genes in these species. Only B. suis is found to have a significant number of unique genes, but combinations of genes and regions that exist in only two out of three genomes and are therefore useful for diagnostics were identified and confirmed. CONCLUSION: Although not all of the differentiating genes identified were transcribed under steady state conditions, a group of genes sufficient to discriminate unambiguously between B. suis, B. melitensis, and B. abortus was identified. We present an overview of these genomic differences and the use of these features to discriminate among a number of Brucella biovars
Accumulation of the common mitochondrial DNA deletion induced by ionizing radiation
AbstractPoint mutations and deletions in mitochondrial DNA (mtDNA) accumulate as a result of oxidative stress, including ionizing radiation. As a result, dysfunctional mitochondria suffer from a decline in oxidative phosphorylation and increased release of superoxides and other reactive oxygen species (ROS). Through this mechanism, mitochondria have been implicated in a host of degenerative diseases. Associated with this type of damage, and serving as a marker of total mtDNA mutations and deletions, the accumulation of a specific 4977-bp deletion, known as the common deletion (Δ-mtDNA4977), takes place. The Δ-mtDNA4977 has been reported to increase with age and during the progression of mitochondrial degeneration. The purpose of this study was to investigate whether ionizing radiation induces the formation of the common deletion in a variety of human cell lines and to determine if it is associated with cellular radiosensitivity. Cell lines used included eight normal human skin fibroblast lines, a radiosensitive non-transformed and an SV40 transformed ataxia telangiectasia (AT) homozygous fibroblast line, a Kearns Sayre Syndrome (KSS) line known to contain mitochondrial deletions, and five human tumor lines. The Δ-mtDNA4977 was assessed by polymerase chain reaction (PCR). Significant levels of Δ-mtDNA4977 accumulated 72 h after irradiation doses of 2, 5, 10 or 20 Gy in all of the normal lines with lower response in tumor cell lines, but the absolute amounts of the induced deletion were variable. There was no consistent dose–response relationship. SV40 transformed and non-transformed AT cell lines both showed significant induction of the deletion. However, the five tumor cell lines showed only a modest induction of the deletion, including the one line that was deficient in DNA damage repair. No relationship was found between sensitivity to radiation-induced deletions and sensitivity to cell killing by radiation
Interleukin-27 Is Essential for Type 1 Diabetes Development and Sjögren Syndrome-like Inflammation.
Human genetic studies implicate interleukin-27 (IL-27) in the pathogenesis of type 1 diabetes (T1D), but the underlying mechanisms remain largely unexplored. To further define the role of IL-27 in T1D, we generated non-obese diabetic (NOD) mice deficient in IL-27 or IL-27Rα. In contrast to wild-type NOD mice, both NOD.Il27-/- and NOD.Il27ra-/- strains are completely resistant to T1D. IL-27 from myeloid cells and IL-27 signaling in T cells are critical for T1D development. IL-27 directly alters the balance of regulatory T cells (Tregs) and T helper 1 (Th1) cells in pancreatic islets, which in turn modulates the diabetogenic activity of CD8 T cells. IL-27 also directly enhances the effector function of CD8 T cells within pancreatic islets. In addition to T1D, IL-27 signaling in T cells is also required for lacrimal and salivary gland inflammation in NOD mice. Our study reveals that IL-27 contributes to autoimmunity in NOD mice through multiple mechanisms and provides substantial evidence to support its pathogenic role in human T1D
Measurement of 92Mo(n,α)89Zr and 97Mo(n,p)97Nb reactions at the neutron energy 13.52 MeV with covariance analysis
218-222The cross sections have been estimated for the Nuclear reactions 92Mo(n,α)89Zr and 97Mo(n,p)97Nb produced in Purnima neutron generator at neutron energy of 13.52±0.0045 MeV using activation analysis and off-line γ -ray spectrometric techniques. 27Al(n,α)24Na has been used as a monitor reaction. The covariance analysis for these cross sections has been carried out by taking into consideration of partial uncertainties of different attributes and correlations between the attributes. The cross section values of the present study have been compared with EXFOR, ENDF data of various libraries and theoretical data of TALYS-1.8 code
Titanium Particles Modulate Lymphocyte and Macrophage Polarization in Peri-Implant Gingival Tissues
Titanium dental implants are one of the modalities to replace missing teeth. The release of titanium particles from the implant’s surface may modulate the immune cells, resulting in implant failure. However, little is known about the immune microenvironment that plays a role in peri-implant inflammation as a consequence of titanium particles. In this study, the peri-implant gingival tissues were collected from patients with failed implants, successful implants and no implants, and then a whole transcriptome analysis was performed. The gene set enrichment analysis confirmed that macrophage M1/M2 polarization and lymphocyte proliferation were differentially expressed between the study groups. The functional clustering and pathway analysis of the differentially expressed genes between the failed implants and successful implants versus no implants revealed that the immune response pathways were the most common in both comparisons, implying the critical role of infiltrating immune cells in the peri-implant tissues. The H&E and IHC staining confirmed the presence of titanium particles and immune cells in the tissue samples, with an increase in the infiltration of lymphocytes and macrophages in the failed implant samples. The in vitro validation showed a significant increase in the level of IL-1β, IL-8 and IL-18 expression by macrophages. Our findings showed evidence that titanium particles modulate lymphocyte and macrophage polarization in peri-implant gingival tissues, which can help in the understanding of the imbalance in osteoblast–osteoclast activity and failure of dental implant osseointegration
Adaptive Marine Predator Optimization Algorithm (AOMA)–Deep Supervised Learning Classification (DSLC)based IDS framework for MANET security
Due to the dynamic nature and node mobility, assuring the security of Mobile Ad-hoc Networks (MANET) is one of the difficult and challenging tasks today. In MANET, the Intrusion Detection System (IDS) is crucial because it aids in the identification and detection of malicious attacks that impair the network’s regular operation. Different machine learning and deep learning methodologies are used for this purpose in the conventional works to ensure increased security of MANET. However, it still has significant flaws, including increased algorithmic complexity, lower system performance, and a higher rate of misclassification. Therefore, the goal of this paper is to create an intelligent IDS framework for significantly enhancing MANET security through the use of deep learning models. Here, the min-max normalization model is applied to preprocess the given cyber-attack datasets for normalizing the attributes or fields, which increases the overall intrusion detection performance of classifier. Then, a novel Adaptive Marine Predator Optimization Algorithm (AOMA) is implemented to choose the optimal features for improving the speed and intrusion detection performance of classifier. Moreover, the Deep Supervise Learning Classification (DSLC) mechanism is utilized to predict and categorize the type of intrusion based on proper learning and training operations. During evaluation, the performance and results of the proposed AOMA-DSLC based IDS methodology is validated and compared using various performance measures and benchmarking datasets
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