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In this work, we present the Genome Modeling System (GMS), an analysis information management system capable of executing automated genome analysis pipelines at a massive scale. The GMS framework provides detailed tracking of samples and data coupled with reliable and repeatable analysis pipelines. The GMS also serves as a platform for bioinformatics development, allowing a large team to collaborate on data analysis, or an individual researcher to leverage the work of others effectively within its data management system. Rather than separating ad-hoc analysis from rigorous, reproducible pipelines, the GMS promotes systematic integration between the two. As a demonstration of the GMS, we performed an integrated analysis of whole genome, exome and transcriptome sequencing data from a breast cancer cell line (HCC1395) and matched lymphoblastoid line (HCC1395BL). These data are available for users to test the software, complete tutorials and develop novel GMS pipeline configurations. The GMS is available at https://github.com/genome/gms.

Hacker Code will have over 400 pages of dedicated exploit, vulnerability, and tool code with corresponding instruction. Unlike other security and programming books that dedicate hundreds of pages to architecture and theory based flaws and exploits, HC1 will dive right into deep code analysis. Previously undisclosed security research in combination with superior programming techniques from Foundstone and other respected organizations will be included in both the Local and Remote Code sections of the book. The book will be accompanied with a FREE COMPANION CD containing both commented and uncommented versions of the source code examples presented throughout the book. In addition to the book source code, the CD will also contain a copy of the author-developed Hacker Code Library v1.0. The Hacker Code Library will include multiple attack classes and functions that can be utilized to quickly create security programs and scripts. These classes and functions will simplify exploit and vulnerability tool development to an extent never before possible with publicly available software. * Learn to quickly create security tools that ease the burden of software testing and network administration* Find out about key security issues regarding vulnerabilities, exploits, programming flaws, and secure code development * Discover the differences in numerous types of web-based attacks so that developers can create proper quality assurance testing procedures and tools* Learn to automate quality assurance, management, and development tasks and procedures for testing systems and applications* Learn to write complex Snort rules based solely upon traffic generated by network tools and exploits

User passwords are the keys to the network kingdom, yet most users choose overly simplistic passwords (like password) that anyone could guess, while system administrators demand impossible to remember passwords littered with obscure characters and random numerals.Every computer user must face the problems of password security.

In this work, we present the Genome Modeling System (GMS), an analysis information management system capable of executing automated genome analysis pipelines at a massive scale. The GMS framework provides detailed tracking of samples and data coupled with reliable and repeatable analysis pipelines. The GMS also serves as a platform for bioinformatics development, allowing a large team to collaborate on data analysis, or an individual researcher to leverage the work of others effectively within its data management system. Rather than separating ad-hoc analysis from rigorous, reproducible pipelines, the GMS promotes systematic integration between the two. As a demonstration of the GMS, we performed an integrated analysis of whole genome, exome and transcriptome sequencing data from a breast cancer cell line (HCC1395) and matched lymphoblastoid line (HCC1395BL). These data are available for users to test the software, complete tutorials and develop novel GMS pipeline configurations. The GMS is available at https://github.com/genome/gms.

This book is about software piracy--what it is and how it's done.Stealing software is not to be condoned, and theft of intellectual property and copyright infringement are serious matters, but it's totally unrealistic to pretend that it doesn't happen.Software piracy has reached epidemic proportions.

Written by Microsoft's Log Parser developer, this is the first book available on Microsoft's popular yet undocumented log parser tool. The book and accompanying Web site contain hundreds of customized, working scripts and templates that system administrators will find invaluable for analyzing the log files from Windows Server, Snort IDS, ISA Server, IIS Server, Exchange Server, and other products.System administrators running Windows, Unix, and Linux networks manage anywhere from 1 to thousands of operating systems (Windows, Unix, etc.), Applications (Exchange, Snort, IIS, etc.), and hardware devices (firewalls, routers, etc.) that generate incredibly long and detailed log files of all activity on the particular application or device. This book will teach administrators how to use Microsoft's Log Parser to data mine all of the information available within these countless logs. The book teaches readers how all queries within Log Parser work (for example: a Log Parser query to an Exchange log may provide information on the origin of spam, viruses, etc.). Also, Log Parser is completely scriptable and customizable so the book will provide the reader with hundreds of original, working scripts that will automate these tasks and provide formatted charts and reports detailing the results of the queries.Written by Microsoft's sole developer of Log Parser, this is the first book available on the powerful yet completely undocumented product that ships with Microsoft's IIS, Windows Advanced Server 2003, and is available as a free download from the Microsoft Web siteThis book and accompanying scripts will save system administrators countless hours by scripting and automating the most common to the most complex log analysis tasks

Abstract Rationale Little is known regarding the impact of ambient ultrafine particles (UFPs; <0.1 μm) on childhood asthma development. Objectives To examine the association between prenatal and early postnatal life exposure to UFPs and development of childhood asthma. Methods A total of 160,641 singleton live births occurring in the City of Toronto, Canada between April 1, 2006, and March 31, 2012, were identified from a birth registry. Associations between exposure to ambient air pollutants and childhood asthma incidence (up to age 6) were estimated using random effects Cox proportional hazards models, adjusting for personal- and neighborhood-level covariates. We investigated both single-pollutant and multipollutant models accounting for coexposures to particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5) and NO2. Measurements and Main Results We identified 27,062 children with incident asthma diagnosis during the follow-up. In adjusted models, second-trimester exposure to UFPs (hazard ratio per interquartile range increase, 1.09; 95% confidence interval, 1.06–1.12) was associated with asthma incidence. In models additionally adjusted for PM2.5 and nitrogen dioxide, UFPs exposure during the second trimester of pregnancy remained positively associated with childhood asthma incidence (hazard ratio per interquartile range increase, 1.05; 95% confidence interval, 1.01–1.09). Conclusions This is the first study to evaluate the association between perinatal exposure to UFPs and the incidence of childhood asthma. Exposure to UFPs during a critical period of lung development was linked to the onset of asthma in children, independent of PM2.5 and NO2.

Old age and FMS-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) mutations in patients with acute myeloid leukaemia are associated with early relapse and poor survival. Quizartinib is an oral, highly potent, and selective next-generation FLT3 inhibitor with clinical antileukaemic activity in relapsed or refractory acute myeloid leukaemia. We aimed to assess the efficacy and safety of single-agent quizartinib in patients with relapsed or refractory acute myeloid leukaemia. We did an open-label, multicentre, single-arm, phase 2 trial at 76 hospitals and cancer centres in the USA, Europe, and Canada. We enrolled patients with morphologically documented primary acute myeloid leukaemia or acute myeloid leukaemia secondary to myelodysplastic syndromes and an Eastern Cooperative Oncology Group (ECOG) performance status of 0–2 into two predefined, independent cohorts: patients who were aged 60 years or older with relapsed or refractory acute myeloid leukaemia within 1 year after first-line therapy (cohort 1), and those who were 18 years or older with relapsed or refractory disease following salvage chemotherapy or haemopoietic stem cell transplantation (cohort 2). Patients with an FLT3-ITD allelic frequency of more than 10% were considered as FLT3-ITD positive, whereas all other patients were considered as FLT3-ITD negative. Patients received quizartinib once daily as an oral solution; the initial 17 patients received 200 mg per day but the QTcF interval was prolonged for more than 60 ms above baseline in some of these patients. Subsequently, doses were amended for all patients to 135 mg per day for men and 90 mg per day for women. The co-primary endpoints were the proportion of patients who achieved a composite complete remission (defined as complete remission + complete remission with incomplete platelet recovery + complete remission with incomplete haematological recovery) and the proportion of patients who achieved a complete remission. Efficacy and safety analyses included all patients who received at least one dose of quizartinib (ie, the intention-to-treat population). Patients with a locally assessed post-treatment bone marrow aspirate or biopsy were included in efficacy analyses by response; all other patients were considered to have an unknown response. This study is registered with ClinicalTrials.gov, number NCT00989261, and with the European Clinical Trials Database, EudraCT 2009-013093-41, and is completed. Between Nov 19, 2009, and Oct 31, 2011, a total of 333 patients were enrolled (157 in cohort 1 and 176 in cohort 2). In cohort 1, 63 (56%) of 112 FLT3-ITD-positive patients and 16 (36%) of 44 FLT3-ITD-negative patients achieved composite complete remission, with three (3%) FLT3-ITD-positive patients and two (5%) FLT3-ITD-negative patients achieving complete remission. In cohort 2, 62 (46%) of 136 FLT3-ITD-positive patients achieved composite complete remission with five (4%) achieving complete remission, whereas 12 (30%) of 40 FLT3-ITD-negative patients achieved composite complete remission with one (3%) achieving complete remission. Across both cohorts (ie, the intention-to-treat population of 333 patients), grade 3 or worse treatment-related treatment-emergent adverse events in 5% or more of patients were febrile neutropenia (76 [23%] of 333), anaemia (75 [23%]), thrombocytopenia (39 [12%]), QT interval corrected using Fridericia's formula (QTcF) prolongation (33 [10%]), neutropenia (31 [9%]), leucopenia (22 [7%]), decreased platelet count (20 [6%]), and pneumonia (17 [5%]). Serious adverse events occurring in 5% or more of patients were febrile neutropenia (126 [38%] of 333; 76 treatment related), acute myeloid leukaemia progression (73 [22%]), pneumonia (40 [12%]; 14 treatment related), QTcF prolongation (33 [10%]; 32 treatment related), sepsis (25 [8%]; eight treatment related), and pyrexia (18 [5%]; nine treatment related). Notable serious adverse events occurring in less than 5% of patients were torsades de pointes (one [<1%]) and hepatic failure (two [1%]). In total, 125 (38%) of 333 patients died within the study treatment period, including the 30-day follow-up. 18 (5%) patients died because of an adverse event considered by the investigator to be treatment related (ten [6%] of 157 patients in cohort 1 and eight [5%] of 176 in cohort 2. Single-agent quizartinib was shown to be highly active and generally well tolerated in patients with relapsed or refractory acute myeloid leukaemia, particularly those with FLT3-ITD mutations. These findings confirm that targeting the FLT3-ITD driver mutation with a highly potent and selective FLT3 inhibitor is a promising clinical strategy to help improve clinical outcomes in patients with very few options. Phase 3 studies (NCT02039726; NCT02668653) will examine quizartinib at lower starting doses. Ambit Biosciences/Daiichi Sankyo.

Previous studies on performance effects by New Zealand blackcurrant (NZBC) extract used mainly a single exercise task. We examined the effects of NZBC extract in a battery of rugby union–specific tests including speed, agility and strength testing. University male rugby union players (n = 13, age: 21 ± 2 years, height: 182 ± 6 cm, body mass: 87 ± 13 kg) completed two full familiarisations and two experimental visits in an indoor facility. The study had a double blind, placebo-controlled, randomised, crossover design. For the experimental visits, participants consumed NZBC extract (210 mg/day of anthocyanins for 7 days) or placebo with a 7-day wash-out. Testing order was the running-based anaerobic sprint test, the Illinois agility test, seated medicine ball (3 kg) throw, and handgrip strength. With NZBC extract, there may have been an effect for average sprint time to be faster by 1.7% (placebo: 5.947 ± 0.538 s, NZBC extract: 5.846 ± 0.571 s, d = −0.18 (trivial), p = 0.06). However, with NZBC extract there may have been reduced slowing of sprint 2 (d = −0.59 (moderate), p = 0.06) and reduced slowing for sprint 6 (d = −0.56 (moderate), p = 0.03). In the Illinois agility test, there may have also been an effect for the mean time to be faster by 1.6% (placebo: 18.46 ± 1.44 s, NZBC extract: 18.15 ± 1.22 s, d = −0.24 (small), p = 0.07). The correlation between the %change in average sprint time and %change in mean agility time was not significant (Pearson R2 = 0.0698, p = 0.383). There were no differences for the seated medicine ball throw distance (p = 0.106) and handgrip strength (p = 0.709). Intake of NZBC extract in rugby union players seems to improve tasks that require maximal speed and agility but not muscle strength. NZBC blackcurrant extract may be able to enhance exercise performance in team sports that require repeated movements with high intensity and horizontal change of body position without affecting muscle strength.

Here we show how major rivers can efficiently connect to the deep-sea, by analysing the longest runout sediment flows (of any type) yet measured in action on Earth. These seafloor turbidity currents originated from the Congo River-mouth, with one flow travelling >1,130 km whilst accelerating from 5.2 to 8.0 m/s. In one year, these turbidity currents eroded 1,338-2,675 [>535-1,070] Mt of sediment from one submarine canyon, equivalent to 19–37 [>7–15] % of annual suspended sediment flux from present-day rivers. It was known earthquakes trigger canyon-flushing flows. We show river-floods also generate canyon-flushing flows, primed by rapid sediment-accumulation at the river-mouth, and sometimes triggered by spring tides weeks to months post-flood. It is demonstrated that strongly erosional turbidity currents self-accelerate, thereby travelling much further, validating a long-proposed theory. These observations explain highly-efficient organic carbon transfer, and have important implications for hazards to seabed cables, or deep-sea impacts of terrestrial climate change. This paper analyses the longest sediment flows measured in action on Earth. These seabed flows were caused by floods and spring tides, and flushed prodigious sediment and carbon volumes into the deep sea, as they accelerated for a thousand kilometres.