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, states that no person convicted of an offence under section 121 (frauds on the Government), section 124 (selling or purchasing office), section 380 (Fraud - if directed against Her Majesty) or section 418 (selling defective stores to Her Majesty), has, after that conviction, the capacity to contract with Her Majesty or to receive any benefits under a contract between Her Majesty and any other person or to hold office under Her Majesty unless a pardon has been granted. (This effectively prohibits granting of a Reliability Status to any such individual.) [9]

Further information: Security vetting in the United Kingdom

National Security Clearances are a hierarchy of five levels, depending on the classification of materials that can be accessed — Baseline Personnel Security Standard (BPSS), Counter-Terrorist Check (CTC), Enhanced Baseline Standard (EBS), Security Check (SC) and Developed Vetting (DV).

The BPSS is the entry-level National Security Clearance, and both CTC and EBS are effectively enhancements to the BPSS, with CTC relating to checking for susceptibility to extremist persuasion, and EBS relating to checking for susceptibility to espionage persuasion, the latter being needed for supervised access to SECRET material. The SC again is focused on susceptibility to espionage persuasion, and is required for an individual to have long-term unsupervised access to SECRET material and occasional access to TOP SECRET (TS) material, whilst for regular access to TS the DV is required.

Those with National Security Clearance are commonly required to sign a statement to the effect that they agree to abide by the restrictions of the Official Secrets Act (OSA). This is popularly referred to as "signing the Official Secrets Act". Signing this has no effect on which actions are legal, as the act is a law, not a contract, and individuals are bound by it whether or not they have signed it. Signing it is intended more as a reminder to the person that they are under such obligations. To this end, it is common to sign this statement both before and after a period of employment that involves access to secrets.

After the United States entered into World War II , Britain changed its security classifications to match those of the U.S.. Previously, classifications had included the top classification "Most Secret", but it soon became apparent that the United States did not fully understand the UK's classifications, and classified information appeared in the U.S.'s press. This spearheaded the uniformity in classification between the United Kingdom and the United States.

In addition to National Security Clearances, other types of roles and organisations stipulate a need for clearances, including:

An algorithm specifies a series of steps that perform a particular computation or task. Algorithms were originally born as part of mathematics – the word “algorithm” comes from the Arabic writer Muḥammad ibn Mūsā al-Khwārizmī, – but currently the word is strongly associated with computer science. Throughout this book we’ll examine a number of different algorithms to perform a variety of tasks.

Algorithms resemble recipes. Recipes tell you how to accomplish a task by performing a number of steps. For example, to bake a cake the steps are: preheat the oven; mix flour, sugar, and eggs throughly; pour into a baking pan; and so forth.

However, “algorithm” is a technical term with a more specific meaning than “recipe”, and calling something an algorithm means that the following properties are all true:

Studying algorithms is a fundamental part of computer science. There are several different characteristics of an algorithm that are useful to know:

Most of these questions will be discussed for the algorithms covered in this book.

An Example Algorithm

Let’s look at a very simple algorithm called find_max() .

Problem: Given a list of positive numbers, return the largest number on the list.

Inputs: A list L of positive numbers. This list must contain at least one number. (Asking for the largest number in a list of no numbers is not a meaningful question.)

Outputs: A number n , which will be the largest number of the list.


An implementation in Python:

Does this meet the criteria for being an algorithm?

There can be many different algorithms for solving the same problem. Here’s an alternative algorithm for find_max() :


Let’s ask our questions again.

Is it unambiguous? Yes. Each step is simple and easily translated into Python.

Does it have defined inputs and outputs? Yes.

Is it guaranteed to terminate? Yes. The algorithm obviously terminates if L is of length 1. If L has more than one element, find_max() is called with a list that’s one element shorter and the result is used in a computation.

Does the nested call to find_max() always terminate? Yes. Each time, find_max() is called with a list that’s shorter by one element, so eventually the list will be of length 1 and the nested calls will end.

Finally, does it produce the correct result? Yes. Here’s a sketch of a proof. [2]

Consider a list of length 1. In this case the largest number is also the only number on the list. find_max() returns this number, so it’s correct for lists of length 1.


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Our two novel findings relating to the relationship between gene expression variation and clinical syndromes associated with CAD are 1) demonstration of a clear transcriptomic signature of AMI that is indicative of a pro-inflammatory response, and 2) that a subset of this axis of peripheral blood gene expression is likely associated with the risk of cardiovascular death during medium-term follow-up [ 32 ]. Importantly, the PC1 gene score added predictive value to standard risk factors, with a hazard ratio over 8 in a multivariate model, and demonstrated improvement in the standard C-statistic. Moreover, our key results are based on replication in two independent phases of genomic data acquisition in the Emory Cardiovascular Biobank, and have been validated using two parallel modes of data normalization. Other findings are a lack of association between the transcriptome and the presence and severity of CAD, occurrence of previous MI, or with cardiovascular medication use.

We found an unambiguous association between a pro-inflammatory gene expression profile and presentation with AMI. The fact that samples were drawn within 2 to 24 hours after AMI, and that the two associated axes of variation (axis 5 and axis 1) are heavily enriched for upregulation of neutrophil and downregulation of T-lymphocyte gene activity, respectively, suggest that this pattern of gene expression may have been the result of AMI rather than its cause. However, these observations may not be entirely explained by neutrophilia that accompanies AMI [ 33 , 34 ]. First, not all neutrophil- and T-lymphocyte-enriched transcripts were altered to the same extent. Thus, in addition to modification of the ratio of cell types, there is differential activation of the co-regulated innate and adaptive gene functions. Secondly, 20% of the eQTL effects are stronger in subjects without AMI than in those with AMI, indicating altered genetic regulation of gene expression. Thus, we conclude that AMI is associated not just with an increase in neutrophil activity, but also with an alteration of gene activity in both neutrophils and lymphoctyes.Our results suggest that there may be a specific subset of leukocyte gene activity that is associated with a particularly high risk of death among individuals with CAD. Our current sample is too small to evaluate whether genotypic differences contribute to this risk category. We do not see any enrichment for eQTL in these genes, but the finding that genotypes affect response to a cardiac event also raises the question of whether enrichment with certain genotypes affects an individual’s physiological response to AMI. Just as with genome-wide association studies, it will likely take joint gene expression and whole genome genotype studies of tens of thousands of individuals with CAD to identify robust genomic biomarkers of risk for adverse events. This signature is, to some extent, co-regulated by whatever processes result in coordinate expression of genes in axis 1 and axis 5, but appears to involve additional coordinated regulation of transcription of a subset of genes with diverse molecular functions. Although the cardiovascular death signature appears to be related to that of AMI, it is only a subset of it, since comparison of Figure 5 A,B with Figure 5 D indicates that the transcripts most strongly associated with death in both phases are only weakly associated with AMI. Both the AMI and cardiovascular death associations are in the same direction in individuals who experienced a follow-up non-lethal MI, further indicating that there is some commonality to the cellular and transcriptional bases to the gene expression-based risk of adverse cardiovascular events.

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