Detecting SPIT Attacks in VoIP Networks Using Convolutional Autoencoders: A Deep Learning Approach

Voice over Internet Protocol (VoIP) is a technology that enables voice communication to be transmitted over the Internet, transforming communication in both personal and business contexts by offering several benefits such as cost savings and integration with other communication systems. However, VoIP attacks are a growing concern for organizations that rely on this technology for communication. Spam over Internet Telephony (SPIT) is a type of VoIP attack that involves unwanted calls or messages, which can be both annoying and pose security risks to users. Detecting SPIT can be challenging since it is often delivered from anonymous VoIP accounts or spoofed phone numbers. This paper suggests an anomaly detection model that utilizes a deep convolutional autoencoder to identify SPIT attacks. The model is trained on a dataset of normal traffic and then encodes new traffic into a lower-dimensional latent representation. If the network traffic varies significantly from the encoded normal traffic, the model flags it as anomalous. Additionally, the model was tested on two datasets and achieved F1 scores of 99.32% and 99.56%. Furthermore, the proposed model was compared to several traditional anomaly detection approaches and it outperformed them on both datasets

Specific behavioral and cellular adaptations induced by chronic morphine are reduced by dietary omega-3 polyunsaturated fatty acids

Opiates, one of the oldest known drugs, are the benchmark for treating pain. Regular opioid exposure also induces euphoria making these compounds addictive and often misused, as shown by the current epidemic of opioid abuse and overdose mortalities. In addition to the effect of opioids on their cognate receptors and signaling cascades, these compounds also induce multiple adaptations at cellular and behavioral levels. As omega-3 polyunsaturated fatty acids (n-3 PUFAs) play a ubiquitous role in behavioral and cellular processes, we proposed that supplemental n-3 PUFAs, enriched in docosahexanoic acid (DHA), could offset these adaptations following chronic opioid exposure. We used an 8 week regimen of n-3 PUFA supplementation followed by 8 days of morphine in the presence of this diet. We first assessed the effect of morphine in different behavioral measures and found that morphine increased anxiety and reduced wheel-running behavior. These effects were reduced by dietary n-3 PUFAs without affecting morphine-induced analgesia or hyperlocomotion, known effects of this opiate acting at mu opioid receptors. At the cellular level we found that morphine reduced striatal DHA content and that this was reversed by supplemental n-3 PUFAs. Chronic morphine also increased glutamatergic plasticity and the proportion of Grin2B-NMDARs in striatal projection neurons. This effect was similarly reversed by supplemental n-3 PUFAs. Gene analysis showed that supplemental PUFAs offset the effect of morphine on genes found in neurons of the dopamine receptor 2 (D2)-enriched indirect pathway but not of genes found in dopamine receptor 1(D1)-enriched direct-pathway neurons. Analysis of the D2 striatal connectome by a retrogradely transported pseudorabies virus showed that n-3 PUFA supplementation reversed the effect of chronic morphine on the innervation of D2 neurons by the dorsomedial prefontal and piriform cortices. Together these changes outline specific behavioral and cellular effects of morphine that can be reduced or reversed by dietary n-3 PUFAs

Specific behavioral and cellular adaptations induced by chronic morphine are reduced by dietary omega-3 polyunsaturated fatty acids.

Opiates, one of the oldest known drugs, are the benchmark for treating pain. Regular opioid exposure also induces euphoria making these compounds addictive and often misused, as shown by the current epidemic of opioid abuse and overdose mortalities. In addition to the effect of opioids on their cognate receptors and signaling cascades, these compounds also induce multiple adaptations at cellular and behavioral levels. As omega-3 polyunsaturated fatty acids (n-3 PUFAs) play a ubiquitous role in behavioral and cellular processes, we proposed that supplemental n-3 PUFAs, enriched in docosahexanoic acid (DHA), could offset these adaptations following chronic opioid exposure. We used an 8 week regimen of n-3 PUFA supplementation followed by 8 days of morphine in the presence of this diet. We first assessed the effect of morphine in different behavioral measures and found that morphine increased anxiety and reduced wheel-running behavior. These effects were reduced by dietary n-3 PUFAs without affecting morphine-induced analgesia or hyperlocomotion, known effects of this opiate acting at mu opioid receptors. At the cellular level we found that morphine reduced striatal DHA content and that this was reversed by supplemental n-3 PUFAs. Chronic morphine also increased glutamatergic plasticity and the proportion of Grin2B-NMDARs in striatal projection neurons. This effect was similarly reversed by supplemental n-3 PUFAs. Gene analysis showed that supplemental PUFAs offset the effect of morphine on genes found in neurons of the dopamine receptor 2 (D2)-enriched indirect pathway but not of genes found in dopamine receptor 1(D1)-enriched direct-pathway neurons. Analysis of the D2 striatal connectome by a retrogradely transported pseudorabies virus showed that n-3 PUFA supplementation reversed the effect of chronic morphine on the innervation of D2 neurons by the dorsomedial prefontal and piriform cortices. Together these changes outline specific behavioral and cellular effects of morphine that can be reduced or reversed by dietary n-3 PUFAs

Specific behavioral and cellular adaptations induced by chronic morphine are reduced by dietary omega-3 polyunsaturated fatty acids

<div><p>Opiates, one of the oldest known drugs, are the benchmark for treating pain. Regular opioid exposure also induces euphoria making these compounds addictive and often misused, as shown by the current epidemic of opioid abuse and overdose mortalities. In addition to the effect of opioids on their cognate receptors and signaling cascades, these compounds also induce multiple adaptations at cellular and behavioral levels. As omega-3 polyunsaturated fatty acids (n-3 PUFAs) play a ubiquitous role in behavioral and cellular processes, we proposed that supplemental n-3 PUFAs, enriched in docosahexanoic acid (DHA), could offset these adaptations following chronic opioid exposure. We used an 8 week regimen of n-3 PUFA supplementation followed by 8 days of morphine in the presence of this diet. We first assessed the effect of morphine in different behavioral measures and found that morphine increased anxiety and reduced wheel-running behavior. These effects were reduced by dietary n-3 PUFAs without affecting morphine-induced analgesia or hyperlocomotion, known effects of this opiate acting at mu opioid receptors. At the cellular level we found that morphine reduced striatal DHA content and that this was reversed by supplemental n-3 PUFAs. Chronic morphine also increased glutamatergic plasticity and the proportion of Grin2B-NMDARs in striatal projection neurons. This effect was similarly reversed by supplemental n-3 PUFAs. Gene analysis showed that supplemental PUFAs offset the effect of morphine on genes found in neurons of the dopamine receptor 2 (D2)-enriched indirect pathway but not of genes found in dopamine receptor 1(D1)-enriched direct-pathway neurons. Analysis of the D2 striatal connectome by a retrogradely transported pseudorabies virus showed that n-3 PUFA supplementation reversed the effect of chronic morphine on the innervation of D2 neurons by the dorsomedial prefontal and piriform cortices. Together these changes outline specific behavioral and cellular effects of morphine that can be reduced or reversed by dietary n-3 PUFAs.</p></div

The expression of genes enriched in D2-, but not D1-, enriched striatal neurons are altered by both supplemental DHA and morphine.

<p><b>A. D1</b> DHA supplementation did not alter the morphine-induced increase in D1 transcript levels. a, c, d; p<0.001, b; p< 0.05. <b>B. Dyn</b> Neither morphine nor DHA altered the expression of Dyn, a gene enriched in D1-neurons. <b>C. Drd2</b> Morphine reduced D2 expression while DHA supplementation increased D2 expression following saline or morphine, a; p<0.0, b; p<0.05, c; p<0.001.<b>D. Enk</b> Morphine increased the expression of Enk, a D2-enriched gene. This was reduced following DHA in either morphine or saline treated mice. a; p<0.01, b; p<0.05.</p

DHA supplementation attenuates the anxiety induced by morphine without altering analgesia or locomotion, established effects of this opiate.

<p><b>A. Wheel running</b> activity was measured over 16h; 3h of light, 12h of dark, 1h of light. The distance run (cm) every hour is shown in the 3 left panels and the total distance run in the column graphs on the right. DHA supplementation did not alter wheel running in male mice receiving saline (Ai) which by day 8 had increased their activity compared with day 1. *, # p<0.05 vs pre-saline injection activity, shown in the solid (control diet) or dashed (DHA group) lines, of the same treatment. B. Total distance run, depicted in the column graphs, shows that morphine reduced wheel running in both DHA and control groups when compared with pre-treatment levels; **, *** p<0.05 and 0.005 respectively vs basal activity in the control group. ##, ### p<0.05 and 0.005 respectively vs basal activity in the DHA group. However, the hourly time bin data show that DHA attenuated this reduction at specific time-points, 5 and 15 h post-morphine injection on day 1, and 5 hours on day 8, *p<0.05, ***p<0.001 vs control morphine at the same timepoint. <b>B. Elevated Plus Maze (EPM).</b> The time spent and frequency of entry into the second, outer half of the EPM was assessed 5h following the last injection of the 8^th day of the morphine or saline injection protocol. Mice on the control diet receiving morphine spent less time and entered less into this region than control mice receiving saline. Supplemental DHA partially reversed this profile. *, ***p<0.05 and 0.001 respectively vs the control saline group, #p<0.05 vs control saline and control morphine. <b>C. Morphine-induced analgesia.</b> The effect of DHA on morphine-induced thermal analgesia was assessed by the tail immersion test at 49.5°C. There was no effect of diet on basal tail-flick latency. Morphine (10mg/kg s.c.) delayed this response in both control and DHA groups (*** p<0.001 vs baseline measures). <b>D. Morphine induced locomotion.</b> i. This effect if morphine was assessed immediately following the first of the daily morphine injections on days 1, 4 and 8 of the TDA morphine injection protocol. The total distance traveled showed no effect of DHA on either the initial locomotor response, or subsequent, sensitized responses, which increased above saline-treated mice on the matching diet, *p<0.05, ***p<0.001 vs saline of the matching control or DHA diet.</p

Region-specific effects of dietary DHA and morphine on brain DHA content.

<p><b>A. Frontal cortex.</b> DHA supplementation increased DHA content following saline or morphine treatment with no further effect of morphine. a and b; p<0.05. <b>B. Striatum</b>. Chronic morphine decreased DHA tissue content and DHA supplementation increased DHA content following saline or morphine. a; p<0.01, b; p<0.05. c; p<0.0001.</p

Global variation in postoperative mortality and complications after cancer surgery: a multicentre, prospective cohort study in 82 countries

© 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 licenseBackground: 80% of individuals with cancer will require a surgical procedure, yet little comparative data exist on early outcomes in low-income and middle-income countries (LMICs). We compared postoperative outcomes in breast, colorectal, and gastric cancer surgery in hospitals worldwide, focusing on the effect of disease stage and complications on postoperative mortality. Methods: This was a multicentre, international prospective cohort study of consecutive adult patients undergoing surgery for primary breast, colorectal, or gastric cancer requiring a skin incision done under general or neuraxial anaesthesia. The primary outcome was death or major complication within 30 days of surgery. Multilevel logistic regression determined relationships within three-level nested models of patients within hospitals and countries. Hospital-level infrastructure effects were explored with three-way mediation analyses. This study was registered with ClinicalTrials.gov, NCT03471494. Findings: Between April 1, 2018, and Jan 31, 2019, we enrolled 15 958 patients from 428 hospitals in 82 countries (high income 9106 patients, 31 countries; upper-middle income 2721 patients, 23 countries; or lower-middle income 4131 patients, 28 countries). Patients in LMICs presented with more advanced disease compared with patients in high-income countries. 30-day mortality was higher for gastric cancer in low-income or lower-middle-income countries (adjusted odds ratio 3·72, 95% CI 1·70–8·16) and for colorectal cancer in low-income or lower-middle-income countries (4·59, 2·39–8·80) and upper-middle-income countries (2·06, 1·11–3·83). No difference in 30-day mortality was seen in breast cancer. The proportion of patients who died after a major complication was greatest in low-income or lower-middle-income countries (6·15, 3·26–11·59) and upper-middle-income countries (3·89, 2·08–7·29). Postoperative death after complications was partly explained by patient factors (60%) and partly by hospital or country (40%). The absence of consistently available postoperative care facilities was associated with seven to 10 more deaths per 100 major complications in LMICs. Cancer stage alone explained little of the early variation in mortality or postoperative complications. Interpretation: Higher levels of mortality after cancer surgery in LMICs was not fully explained by later presentation of disease. The capacity to rescue patients from surgical complications is a tangible opportunity for meaningful intervention. Early death after cancer surgery might be reduced by policies focusing on strengthening perioperative care systems to detect and intervene in common complications. Funding: National Institute for Health Research Global Health Research Unit