Payload-Byte: A Tool for Extracting and Labeling Packet Capture Files of Modern Network Intrusion Detection Datasets

Adapting modern approaches for network intrusion detection is becoming critical, given the rapid technological advancement and adversarial attack rates. Therefore, packet-based methods utilizing payload data are gaining much popularity due to their effectiveness in detecting certain attacks. However, packet-based approaches suffer from a lack of standardization, resulting in incomparability and reproducibility issues. Unlike flow-based datasets, no standard labeled dataset exists, forcing researchers to follow bespoke labeling pipelines for individual approaches. Without a standardized baseline, proposed approaches cannot be compared and evaluated with each other. One cannot gauge whether the proposed approach is a methodological advancement or is just being benefited from the proprietary interpretation of the dataset. Addressing comparability and reproducibility issues, we introduce Payload-Byte, an open-source tool for extracting and labeling network packets in this work. Payload-Byte utilizes metadata information and labels raw traffic captures of modern intrusion detection datasets in a generalized manner. Moreover, we transformed the labeled data into a byte-wise feature vector that can be utilized for training machine learning models. The whole cycle of processing and labeling is explicitly stated in this work. Furthermore, source code and processed data are made publicly available so that it may act as a standardized baseline for future research work. Lastly, we present a brief comparative analysis of machine learning models trained on packet-based and flow-based data

Axonal plasticity underpins the functional recovery following surgical decompression in a rat model of cervical spondylotic myelopathy.

Cervical spondylotic myelopathy (CSM) is the most common spinal cord disorder and a major cause of disability in adults. Improvements following surgical decompression are limited and patients often remain severely disabled. Post mortem studies indicate that CSM is associated with profound axonal loss. However, our understanding of the pathophysiology of CSM remains limited.To investigate the hypothesis that axonal plasticity plays a role in the recovery following surgical decompression, we adopted a novel preclinical model of mild to moderate CSM. Spinal cord compression resulted in significant locomotor deterioration, increased expression of the axonal injury marker APP, and loss of serotonergic fibres. Surgical decompression partially reversed the deficits and attenuated APP expression. Decompression was also associated with axonal sprouting, reflected in the restoration of serotonergic fibres and an increase of GAP43 expression. The re-expression of synaptophysin indicated the restoration of functional synapses following decompression. Promoting axonal plasticity may therefore be a therapeutic strategy for promoting neurological recovery in CSM.Qatar Foundation, National Institute for Health Research (Clinician Scientist Award Grant ID: CS-2015-15-023), Royal Australasian College of Surgeons (Reg Worcester Research Fellowship), Neurosurgical Society of Australasia (Research Scholarship), Wellcome Trust, Medical Research CouncilThis is the final version of the article. It first appeared from BioMed Central via http://dx.doi.org/10.1186/s40478-016-0359-

Inhibition of CNS remyelination by the presence of semaphorin 3A

Failure of oligodendrocyteprecursor cell (OPC)differentiationhasbeen recognized asthe leading causeforthefailure ofmyelin regenerationin diseases such as multiple sclerosis (MS). One explanation for the failure of OPC differentiation in MS is the presence of inhibitory molecules in demyelinatedlesions.Sofaronly afewinhibitory substrateshavebeenidentifiedinMSlesions.Semaphorin3A (Sema3A), a secretedmemberof the semaphorin family, can act as repulsive guidance cue for neuronal and glial cells in the CNS. Recent studies suggest that Sema3A is also expressedin activeMSlesions.However,theimplicationof Sema3A expressioninMSlesions remainsunclear asOPCs are commonlypresentin chronic demyelinated lesions. In the present study we identify Sema3A as a potent, selective, and reversible inhibitor of OPC differentiation in vitro. Furthermore, we show that administration of Sema3A into demyelinating lesions in the rat CNS results in a failure of remyelination. Our results imply an important role for Sema3A in the differentiation block occurring in MS lesions

COMPARISON OF IRON STORES IN HEALTHY INDIVIDUALS AND PATIENTS WITH ISCHAEMIC HEART DISEASE

ABSTRACT Excess body iron has been linked to atherosclerosis owing to its pro-oxidative properties. However, inconsistent results have emerged from the epidemiological studies linking iron status and the risk of cardiovascular diseases (CVD). Objective of the present study is to compare iron stores of healthy individuals and patients with ischaemic heart disease (IHD). A total of 137 subjects were included in the study, 90 patients of IHD and 47 healthy subjects with no history of IHD as controls. We compared body iron stores of patients and controls. Serum ferritin, serum transferrin receptor (sTfR) and sTfR/ferritin ratio were used as measures of body iron stores. Our results revealed that mean serum ferritin concentration of cases was significantly higher than controls. Moreover, mean sTfR and sTfR/ferritin ratio of controls was significantly higher than the patients. We conclude from our results that IHD patients have higher iron stores than healthy subjects suggesting a possible association between high iron stores and the risk of IHD

In Vitro Release Studies of Diclofenac Potassium Tablet from Pure and Blended Mixture of Hydrophilic and Hydrophobic Polymers

The purpose of the present study was to evaluate the effect of pure and blended mixtures, with different compositions of hydroxy propyl methyl cellulose (HPMC) and carnauba wax (CW) on the release of diclofenac potassium from matrix tablets. Fifteen different matrix tablet formulations were prepared by direct compression process by using Carver Hydraulic laboratory press having 13 mm flat dies set at constant pressure. The paddle dissolution apparatus II (Curio DL 2020) was used to assess the dissolution of drug in phosphate buffer, pH 7.4 for 8 h. The release data was fitted to different release models. Zoom stereo micrography was done to evaluated the release mechanism of drug from polymers. The interaction of polymer mixture and different ratios of drug in polymer mixture was determined by Fourier transform infrared spectroscopy (FTIR) and differential scanning calorimetry (DSC). The type and content of polymer in the matrix system influenced the release characteristics. Higher polymeric content in the matrix decreased the drug release rate because of increased tortuosity and decreased porosity. Retardation of drug release from pure carnauba was higher as compared to that with pure HPMC matrices. The polymers blends controlled drug release pattern effectively. The drug released showed better linearity with Higuchi release kinetics. The Korsmeyer equation revealed n value ranged from 0.388-0.627 or non - Fickian transport mechanism of drug release was predominant. The FTIR and DSC suggested that there were no chemical interaction between drug and polymers.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Correlation between maternal and neonatal blood Vitamin D level; A cross sectional study of 416 participants visiting a tertiary care hospital in Pakistan

In Pakistan there is limited evidence for the levels and relationship of 25 (OH) Vitamin D [25(OH)D] status in pregnant women and their newborns while the association between maternal 25(OH)D and newborn anthropometric measurements remains unexplored. Sociodemographic data was collected from 213 pregnant mothers during their visit to a tertiary care hospital at the time of childbirth. Anthropometric measurements were performed on all mothers and their newborns and blood samples collected from both for 25(OH)D levels. Participants were classified into two groups according to their 25(OH)D status: Sufficient (25(OH)D ≥50nmol/l) and Deficient (25(OH)D 0.05). Our study shows a high prevalence of 25(OH)D deficiency in pregnant women and their newborns and a strong positive association between maternal and newborn 25(OH)D levels. Findings of this study indicate the importance of maintaining sufficient 25(OH)D levels during pregnancy

Copy number variants (CNVs): a powerful tool for iPSC-based modelling of ASD

Patients diagnosed with chromosome microdeletions or duplications, known as copy number variants (CNVs), present a unique opportunity to investigate the relationship between patient genotype and cell phenotype. CNVs have high genetic penetrance and give a good correlation between gene locus and patient clinical phenotype. This is especially effective for the study of patients with neurodevelopmental disorders (NDD), including those falling within the autism spectrum disorders (ASD). A key question is whether this correlation between genetics and clinical presentation at the level of the patient can be translated to the cell phenotypes arising from the neurodevelopment of patient induced pluripotent stem cells (iPSCs). Here, we examine how iPSCs derived from ASD patients with an associated CNV inform our understanding of the genetic and biological mechanisms underlying the aetiology of ASD. We consider selection of genetically characterised patient iPSCs; use of appropriate control lines; aspects of human neurocellular biology that can capture in vitro the patient clinical phenotype; and current limitations of patient iPSC-based studies. Finally, we consider how future research may be enhanced to maximise the utility of CNV patients for research of pathological mechanisms or therapeutic targets

Inhibition of phosphodiesterase-4 promotes oligodendrocyte precursor cell differentiation and enhances CNS remyelination

The increasing effectiveness of new disease-modifying drugs that suppress disease activity in multiple sclerosis has opened up opportunities for regenerative medicines that enhance remyelination and potentially slow disease progression. Although several new targets for therapeutic enhancement of remyelination have emerged, few lend themselves readily to conventional drug development. Here, we used transcription profiling to identify mitogen-activated protein kinase (Mapk) signalling as an important regulator involved in the differentiation of oligodendrocyte progenitor cells (OPCs) into oligodendrocytes. We show in tissue culture that activation of Mapk signalling by elevation of intracellular levels of cyclic adenosine monophosphate (cAMP) using administration of either dibutyryl-cAMP or inhibitors of the cAMP-hydrolysing enzyme phosphodiesterase-4 (Pde4) enhances OPC differentiation. Finally, we demonstrate that systemic delivery of a Pde4 inhibitor leads to enhanced differentiation of OPCs within focal areas of toxin-induced demyelination and a consequent acceleration of remyelination. These data reveal a novel approach to therapeutic enhancement of remyelination amenable to pharmacological intervention and hence with significant potential for translation

Inhibition of phosphodiesterase‐4 promotes oligodendrocyte precursor cell differentiation and enhances CNS

The increasing effectiveness of new disease-modifying drugs that suppress disease activity in multiple sclerosis has opened up opportunities for regenerative medicines that enhance remyelination and potentially slow disease progression. Although several new targets for therapeutic enhancement of remyelination have emerged, few lend themselves readily to conventional drug development. Here, we used transcription profiling to identify mitogen-activated protein kinase (Mapk) signalling as an important regulator involved in the differentiation of oligodendrocyte progenitor cells (OPCs) into oligodendrocytes. We show in tissue culture that activation of Mapk signalling by elevation of intracellular levels of cyclic adenosine monophosphate (cAMP) using administration of either dibutyryl-cAMP or inhibitors of the cAMP-hydrolysing enzyme phosphodiesterase-4 (Pde4) enhances OPC differentiation. Finally, we demonstrate that systemic delivery of a Pde4 inhibitor leads to enhanced differentiation of OPCs within focal areas of toxin-induced demyelination and a consequent acceleration of remyelination. These data reveal a novel approach to therapeutic enhancement of remyelination amenable to pharmacological intervention and hence with significant potential for translation