Using Artificial Neural Network as an Approach to Analyze People Sentiment Level Based on Social Media Data

The internet has become an essential online communication tool for many people today. For a variety of reasons, many researches have been done lately in the field of Artificial Neural Network (ANN) considering people sentiments based on social media data. This analytical study conducted to analyze happiness of Libyan people based on twitter data sets.  Matlab used in this study to code around 1,000 status/comments data. Processing consists of five processes, namely cleansing, Tokenization, case folding, removal stop word, and stemming. The study represents Artificial Neural Network model for the mining of Twitter opinions using an Artificial Neural Network model approach for the abstracting and visualization scheme of Twitter feeds and a classification and prediction approach. This study presented a contribution in the form of proposing a new visualization model for Twitter mood prediction based on the ANN approach

Short-term single treatment of chemotherapy results in the enrichment of ovarian cancer stem cell-like cells leading to an increased tumor burden

Over 80% of women diagnosed with advanced-stage ovarian cancer die as a result of disease recurrence due to failure of chemotherapy treatment. In this study, using two distinct ovarian cancer cell lines (epithelial OVCA 433 and mesenchymal HEY) we demonstrate enrichment in a population of cells with high expression of CSC markers at the protein and mRNA levels in response to cisplatin, paclitaxel and the combination of both. We also demonstrate a significant enhancement in the sphere forming abilities of ovarian cancer cells in response to chemotherapy drugs. The results of these in vitro findings are supported by in vivo mouse xenograft models in which intraperitoneal transplantation of cisplatin or paclitaxel-treated residual HEY cells generated significantly higher tumor burden compared to control untreated cells. Both the treated and untreated cells infiltrated the organs of the abdominal cavity. In addition, immunohistochemical studies on mouse tumors injected with cisplatin or paclitaxel treated residual cells displayed higher staining for the proliferative antigen Ki67, oncogeneic CA125, epithelial E-cadherin as well as cancer stem cell markers such as Oct4 and CD117, compared to mice injected with control untreated cells. These results suggest that a short-term single treatment of chemotherapy leaves residual cells that are enriched in CSC-like traits, resulting in an increased metastatic potential. The novel findings in this study are important in understanding the early molecular mechanisms by which chemoresistance and subsequent relapse may be triggered after the first line of chemotherapy treatment

Moringa oleifera Lam. (family Moringaceae) leaf extract attenuates high-fat diet-induced dyslipidemia and vascular endothelium dysfunction in Wistar albino rats

Purpose: To investigate the protective effect of methanol extract of Moringa oleifera leaves (MEMO) in high-fat diet (HFD)-induced dyslipidemia and vascular endothelium dysfunction. Methods: Dose-dependent attenuating effect of MEMO was tested at doses of 200 and 400 mg/kg/day in an in vivo model of HFD-induced dyslipidemia using rats whereas vascular endothelial reactivity was assessed in isolated rat aorta using ex vivo organ bath setup. Results: MEMO administration in HFD-induced dyslipidemic rats for 3 consecutive weeks, resulted in significant decrease in rat body weight, LW/BW and RFPW/BW ratio when compared to rats treated with HFD only where an increase in body weight was observed. Decrease in the average daily feed intake and significant reductions in waist, Lee index and BMI was also observed after MEMO treatment in HFD-induced dyslipidemic rats. Lipid profile data indicate that HFD group showed significant increase in total cholesterol, triglyceride, LDL and VLDL levels while HDL levels decreased significantly. On the other hand, MEMO treatment improved lipid profile compared to HFD group. Ex-vivo isolated aorta results revealed that MEMO treatment reversed HFD-induced endothelium dysfunction when compared to SD group. Conclusion: MEMO treatment produces dose-dependent improvement in lipid profile and vascular endothelium protection, thereby rationalizing its traditional medicine use in the treatment of dyslipidemia and cardiovascular related endothelial disorders

Microstructure, Elastic and Inelastic Properties of Partially Graphitized Biomorphic Carbons

The microstructural characteristics and amplitude dependences of the Young’s modulus E and internal friction (logarithmic decrement δ) of biocarbon matrices prepared by beech wood carbonization at temperatures Tcarb = 850–1600°C in the presence of a nickelcontaining catalyst have been studied. Using Xray diffraction and electron microscopy, it has been shown that the use of a nickel catalyst during carbon ization results in a partial graphitization of biocarbons at Tcarb ≥ 1000°C: the graphite phase is formed as 50 to 100nm globules at Tcarb = 1000°C and as 0.5 to 3.0μm globules at Tcarb = 1600°C. It has been found that the measured dependences E(Tcarb) and δ(Tcarb) contain three characteristic ranges of variations in the Young’s modulus and logarithmic decrement with a change in the carbonization temperature: E increases and δ decreases in the ranges Tcarb 1300°C; in the range 1000 < Tcarb < 1300°C, E sharply decreases and δ increases. The observed behavior of E(Tcarb) and δ(Tcarb) for biocarbons carbonized in the presence of nickel correlates with the evolution of their microstructure. The largest values of E are obtained for samples with Tcarb = 1000 and 1600°C. However, the samples with Tcarb = 1600°C exhibit a higher suscep tibility to microplasticity due to the presence of a globular graphite phase that is significantly larger in size and total volume.Peer reviewe

Efficacy and safety of the second in-hospital dose of tranexamic acid after receiving the prehospital dose: double-blind randomized controlled clinical trial in a level 1 trauma center

Background: Prehospital administration of tranexamic acid (TXA) to injured patients is increasing worldwide. However, optimal TXA dose and need of a second infusion on hospital arrival remain undetermined. We investigated the efficacy and safety of the second in-hospital dose of TXA in injured patients receiving 1 g of TXA in the prehospital setting. We hypothesized that a second in-hospital dose of TXA improves survival of trauma patients. Methods: A prospective, double-blind, placebo-controlled randomized, clinical trial included adult trauma patients receiving 1 g of TXA in the prehospital settings. Patients were then blindly randomized to Group I (second 1-g TXA) and Group II (placebo) on hospital arrival. The primary outcome was 24-h (early) and 28-day (late) mortality. Secondary outcomes were thromboembolic events, blood transfusions, hospital length of stay (HLOS) and organs failure (MOF). Results: A total of 220 patients were enrolled, 110 in each group. The TXA and placebo groups had a similar early [OR 1.000 (0.062–16.192); p = 0.47] and late mortality [OR 0.476 (95% CI 0.157–1.442), p = 0.18].The cause of death (n = 15) was traumatic brain injury (TBI) in 12 patients and MOF in 3 patients. The need for blood transfusions in the first 24 h, number of transfused blood units, HLOS, thromboembolic events and multiorgan failure were comparable in the TXA and placebo groups. In seriously injured patients (injury severity score > 24), the MTP activation was higher in the placebo group (31.3% vs 11.10%, p = 0.13), whereas pulmonary embolism (6.9% vs 2.9%, p = 0.44) and late mortality (27.6% vs 14.3%, p = 0.17) were higher in the TXA group but did not reach statistical significance. Conclusion: The second TXA dose did not change the mortality rate, need for blood transfusion, thromboembolic complications, organ failure and HLOS compared to a single prehospital dose and thus its routine administration should be revisited in larger and multicenter studies. Trial registration: ClinicalTrials.gov Identifier: NCT03846973

Inhibition of the JAK2/STAT3 pathway in ovarian cancer results in the loss of cancer stem cell-like characteristics and a reduced tumor burden

Background Current treatment of ovarian cancer patients with chemotherapy leaves behind a residual tumor which results in recurrent ovarian cancer within a short time frame. We have previously demonstrated that a single short-term treatment of ovarian cancer cells with chemotherapy in vitro resulted in a cancer stem cell (CSC)-like enriched residual population which generated significantly greater tumor burden compared to the tumor burden generated by control untreated cells. In this report we looked at the mechanisms of the enrichment of CSC-like residual cells in response to paclitaxel treatment. Methods The mechanism of survival of paclitaxel-treated residual cells at a growth inhibitory concentration of 50% (GI50) was determined on isolated tumor cells from the ascites of recurrent ovarian cancer patients and HEY ovarian cancer cell line by in vitro assays and in a mouse xenograft model. Results Treatment of isolated tumor cells from the ascites of ovarian cancer patients and HEY ovarian cancer cell line with paclitaxel resulted in a CSC-like residual population which coincided with the activation of Janus activated kinase 2 (JAK2) and signal transducer and activation of transcription 3 (STAT3) pathway in paclitaxel surviving cells. Both paclitaxel-induced JAK2/STAT3 activation and CSC-like characteristics were inhibited by a low dose JAK2-specific small molecule inhibitor CYT387 (1 μM) in vitro. Subsequent, in vivo transplantation of paclitaxel and CYT387-treated HEY cells in mice resulted in a significantly reduced tumor burden compared to that seen with paclitaxel only-treated transplanted cells. In vitro analysis of tumor xenografts at protein and mRNA levels demonstrated a loss of CSC-like markers and CA125 expression in paclitaxel and CYT387-treated cell-derived xenografts, compared to paclitaxel only-treated cell-derived xenografts. These results were consistent with significantly reduced activation of JAK2 and STAT3 in paclitaxel and CYT387-treated cell-derived xenografts compared to paclitaxel only-treated cell derived xenografts. Conclusions This proof of principle study demonstrates that inhibition of the JAK2/STAT3 pathway by the addition of CYT387 suppresses the ‘stemness’ profile in chemotherapy-treated residual cells in vitro, which is replicated in vivo, leading to a reduced tumor burden. These findings have important implications for ovarian cancer patients who are treated with taxane and/or platinum-based therapies. Keywords: Ovarian carcinoma, Cancer stem cell, Metastasis, Ascites, Chemoresistance, Recurrence, JAK2/STAT3 pathwa

Impact of opioid-free analgesia on pain severity and patient satisfaction after discharge from surgery: multispecialty, prospective cohort study in 25 countries

Background: Balancing opioid stewardship and the need for adequate analgesia following discharge after surgery is challenging. This study aimed to compare the outcomes for patients discharged with opioid versus opioid-free analgesia after common surgical procedures.Methods: This international, multicentre, prospective cohort study collected data from patients undergoing common acute and elective general surgical, urological, gynaecological, and orthopaedic procedures. The primary outcomes were patient-reported time in severe pain measured on a numerical analogue scale from 0 to 100% and patient-reported satisfaction with pain relief during the first week following discharge. Data were collected by in-hospital chart review and patient telephone interview 1 week after discharge.Results: The study recruited 4273 patients from 144 centres in 25 countries; 1311 patients (30.7%) were prescribed opioid analgesia at discharge. Patients reported being in severe pain for 10 (i.q.r. 1-30)% of the first week after discharge and rated satisfaction with analgesia as 90 (i.q.r. 80-100) of 100. After adjustment for confounders, opioid analgesia on discharge was independently associated with increased pain severity (risk ratio 1.52, 95% c.i. 1.31 to 1.76; P &lt; 0.001) and re-presentation to healthcare providers owing to side-effects of medication (OR 2.38, 95% c.i. 1.36 to 4.17; P = 0.004), but not with satisfaction with analgesia (beta coefficient 0.92, 95% c.i. -1.52 to 3.36; P = 0.468) compared with opioid-free analgesia. Although opioid prescribing varied greatly between high-income and low- and middle-income countries, patient-reported outcomes did not.Conclusion: Opioid analgesia prescription on surgical discharge is associated with a higher risk of re-presentation owing to side-effects of medication and increased patient-reported pain, but not with changes in patient-reported satisfaction. Opioid-free discharge analgesia should be adopted routinely

The global burden of cancer attributable to risk factors, 2010-19 : a systematic analysis for the Global Burden of Disease Study 2019

Background Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally. Methods The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk-outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented. Findings Globally, in 2019, the risk factors included in this analysis accounted for 4.45 million (95% uncertainty interval 4.01-4.94) deaths and 105 million (95.0-116) DALYs for both sexes combined, representing 44.4% (41.3-48.4) of all cancer deaths and 42.0% (39.1-45.6) of all DALYs. There were 2.88 million (2.60-3.18) risk-attributable cancer deaths in males (50.6% [47.8-54.1] of all male cancer deaths) and 1.58 million (1.36-1.84) risk-attributable cancer deaths in females (36.3% [32.5-41.3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20.4% (12.6-28.4) and DALYs by 16.8% (8.8-25.0), with the greatest percentage increase in metabolic risks (34.7% [27.9-42.8] and 33.3% [25.8-42.0]). Interpretation The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden. Copyright (C) 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license.Peer reviewe

Reducing the environmental impact of surgery on a global scale: systematic review and co-prioritization with healthcare workers in 132 countries

Abstract Background Healthcare cannot achieve net-zero carbon without addressing operating theatres. The aim of this study was to prioritize feasible interventions to reduce the environmental impact of operating theatres. Methods This study adopted a four-phase Delphi consensus co-prioritization methodology. In phase 1, a systematic review of published interventions and global consultation of perioperative healthcare professionals were used to longlist interventions. In phase 2, iterative thematic analysis consolidated comparable interventions into a shortlist. In phase 3, the shortlist was co-prioritized based on patient and clinician views on acceptability, feasibility, and safety. In phase 4, ranked lists of interventions were presented by their relevance to high-income countries and low–middle-income countries. Results In phase 1, 43 interventions were identified, which had low uptake in practice according to 3042 professionals globally. In phase 2, a shortlist of 15 intervention domains was generated. In phase 3, interventions were deemed acceptable for more than 90 per cent of patients except for reducing general anaesthesia (84 per cent) and re-sterilization of ‘single-use’ consumables (86 per cent). In phase 4, the top three shortlisted interventions for high-income countries were: introducing recycling; reducing use of anaesthetic gases; and appropriate clinical waste processing. In phase 4, the top three shortlisted interventions for low–middle-income countries were: introducing reusable surgical devices; reducing use of consumables; and reducing the use of general anaesthesia. Conclusion This is a step toward environmentally sustainable operating environments with actionable interventions applicable to both high– and low–middle–income countries

Mechanisms of acute brain injury following aneurismal subarachnoid hemorrhage: the role of acute microcirculatory failure. An experimental study in mice.

Background: Aneurismal subarachnoid hemorrhage is the most devastating type of stroke, with two thirds of the affected individuals either die or remain with moderate to severe disability. The majority of patients die during the first few days after subarachnoid hemorrhage (SAH) (Macpherson, Lewsey et al. 2011). This mortality is most likely attributed to a severe, cerebral perfusion pressureindependent reduction of cerebral blood flow (CBF). The mechanisms of this CBF decrease are largely unknown and may be related to disturbances at the - level of the cerebral microcircuiation. This project is an attempt to study the pathophysiological mechanisms by which subarachnoid hemorrhage leads to cerebral perfusion pressure- independent cerebral ischemia. We examined the most widely accepted theory that oxyhemoglobin induced nitric oxide depletion plays a key role in the etiology of cerebral ischemia and brain injury after subarachnoid hemorrhage. In order to achieve this, we investigated any role intravascularfree hemoglobin might play in causing nitrogen oxide depletion by measuring plasma hemoglobin levels after experimental subarachnoid hemorrhage and comparing it with normal animals. We then studied cerebral microcircuiation at 1-3 hours after experimental subarachnoid hemorrhage to check for any ischemic changes at this stage after experimental and, also, to test the correlation between perivascular blood, which served as an index for perivascular hemoglobin, and these ischemic changes. Methods: Subarachnoid hemorrhage was induced in C57/BL6 mice using Circle of Willis endovascular perforation technique (Feiler, Friedrich et al. 2010). Intravital fluorescence microscopy was used to study cerebral microcirculation 1-3 hours after experimental subarachnoid hemorrhage. Plasma hemoglobin-was measured using the spectrophotometric scanning method of Blakney and Dinwoodie. Results: Animals had normal physiological parameters throughout the experimental period. Post-hemorrhagic intracranial pressure (ICP) rose to 91 +/- 29mmHg, indicating a comparable severity of SAH in all animals. 56% of observed cerebral vessels were affected by microvasospasm and microthrombosis. These changes were mainly seen in capillaries and small arterioles. 39% of all vasospasms were detected in vessels with 10-20 pm caliber, 28% of vasospasms occurred in vessels with 20-30 µm caliber and 10% in blood vessels with 30-40 µm diameter. 59% of microthrombi were seen blood vessels37% of them occur in vessels with 10-20 µm calibers. 93% of all microvasospasm are associated with blood in the perivascular space compared to only 7% of vasospasm occurring in the absence of perivascular blood. 79% of microthrombi were observed in vessels coated with perivascular blood, compared to 21% of microthrombi detected in the absence of perivascular blood. Plasma hemoglobin levels at 3 & 24 hours after experimental subarachnoid hemorrhage were similar to levels of plasma hemoglobin in control animals. 72 hours after SAH, the levels are higher in SAH animals but the difference is not statistically significant. Conclusions: As early as 1 hour after subarachnoid hemorrhage there are widespread microvasospasms and microthrombosis affecting cerebral microcirculation. These changes are severe enough and extensive enough to cause early post hemorrhagic cerebral ischemia and to serve as an explanation for early mortality following SAH. Extra- rather than intra-vascular hemoglobin is most likely responsible for cerebral microvasospasm and microthrombosis after experimental subarachnoid hemorrhage.</p