A rtificial intelligence (AI) is defined as 'a field of science and engineering concerned with the computational understanding of what is commonly called intelligent behaviour, and with the creation of artefacts that exhibit such behaviour'.1 Aristotle attempted to formalise 'right thinking' (logic) through his syllogisms (a three part deductive reasoning). Much of the work in the modern era was inspired by this and the early studies on the operation of mind helped to establish contemporary logical thinking. Programs which enable computers to function in the ways, that make people seem intelligent are called artificial intelligent systems. The British mathematician Alan Turing (1950) was one of the founders of modern computer science and AI. He defined intelligent behaviour in a computer as the ability to achieve human-level performance in cognitive tasks, this later became popular as the 'Turing test'.2 Since the middle of the last century, researchers have explored the potential applications of intelligent techniques in every field of medicine.3,4 The application of AI technology in the field of surgery was first successively investigated by Gunn in 1976, when he explored the possibility of diagnosing acute abdominal pain with computer analysis. 5 The last two decades have seen a surge in the interest in medical AI.Modern medicine is faced with the challenge of acquiring, analysing and applying the large amount of knowledge necessary to solve complex clinical problems. The development of medical artificial intelligence has been related to the development of AI programs intended Artificial intelligence in medicine AN

Doxorubicin is considered to be the most effective agent in the treatment of breast cancer patients. Unfortunately, resistance to this agent is common, representing a major obstacle to successful treatment. The identification of novel biomarkers that are able to predict treatment response may allow therapy to be tailored to individual patients. Antibody microarrays provide a powerful new technique, enabling the global comparative analysis of many proteins simultaneously. This technology may identify a panel of proteins to discriminate between drug-resistant and drug-sensitive samples. The Panorama Cell Signaling Antibody Microarray was exploited to analyze the MDA-MB-231 breast cancer cell line and a novel derivative, which displays significant resistance to doxorubicin at clinically relevant concentrations. The microarray comprised 224 antibodies selected from a variety of pathways, including apoptotic and cell signaling pathways. A standard z2.0-fold cutoff value was used to determine differentially expressed proteins. A decrease in the expression of mitogen-activated protein kinaseactivated monophosphotyrosine (phosphorylated extracellular signal-regulated kinase; 2.8-fold decrease), cyclin D2 (2.5-fold decrease), cytokeratin 18 (2.5-fold decrease), cyclin B1 (2.4-fold decrease), and heterogeneous nuclear ribonucleoprotein m3-m4 (2.0-fold decrease) was associated with doxorubicin resistance. Western blotting was exploited to confirm results from the antibody microarray experiment. These results suggest that antibody microarrays can be used to identify novel biomarkers and further validation may reveal mechanisms of chemotherapy resistance and identify potential therapeutic targets.

The objective of this study is to estimate the cost of wound care in a local population of approximately 590 000 using results from a wound care audit carried out in Hull and the East Riding of Yorkshire as a basis. Full results of the audit will be published separately. An audit in June 2005 provided information on patients with wounds and on their treatment. This was combined with representative National Health Service unit costs to produce an estimate of the total cost of wound care in 2005-2006. In all, 1644 patients had a total of 2300 wounds (1.44 per patient). Most (74.1%) were treated in the community by district nurses, 21.2% were treated in hospital and 4.8% were treated in residential or hospice care. More than one in four hospital inpatients (26.8%) had a wound. Median duration was 6-12 weeks. Twenty-four per cent had their wound for 6 months or more, and almost 16% of patients had remained unhealed for a year or longer. One in eight wounds (12.8%) were reported as showing signs of infection. The estimated cost of wound care in 2005-2006 was pound15 million to pound18 million ( pound2.5 million to pound3.1 million per 100 000 population). Caring for patients with wounds required the equivalent of 88.5 full-time nurses and up to 87 hospital beds. Wounds are a significant source of cost to patients as well as the health care system. The most important determinant of cost appears to be wound complications which require hospitalisation or which delay hospital discharge. Reducing costs requires a systematic focus on effective and timely diagnosis, on ensuring treatment is appropriate to the cause and condition of the wound and on active measures to prevent complications and wound-related hospitalisation. These results should be generalisable to other similar populations in the UK and elsewhere.

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It has been postulated that the rapid enhancement demonstrated by breast carcinomas after administration of contrast media is a direct result of tumor angiogenesis. However, to date, little quantitative data have been published to support this view. A retrospective study has been undertaken to compare dynamic contrast-enhanced data obtained from 40 patients with microvessel density (MVD) evaluated in specimens immunohistochemically stained with a factor VIII related antigen. The dynamic data were analyzed quantitatively using both simple indices of enhancement and a two-compartment kinetic model. A moderate but significant correlation was demonstrated between initial enhancement and MVD, and this correlation strengthened when node-positive tumors were considered in isolation (r = .77, P < .0005). However, the data showed considerable variability. The enhancement characteristics of the tumors could not be explained solely by their MVD; therefore, MRI cannot be used to predict MVD in vivo. Further work is required to address the exact relationship between contrast-enhanced MRI and tumor angiogenesis.

Wounds represent a significant cause of morbidity in the general population.A systematic focus is necessary on effective and timely diagnosis, on ensuring treatment is appropriate to the cause and condition of the wound and on active measures to prevent complications.A number of initiatives have commenced in order to provide a effective and efficient wound care.

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CD40–CD40L interactions play a critical role in regulating immune responses. Blockade of CD40L by Abs, such as the anti-CD40L Ab 5c8, demonstrated positive clinical effects in patients with autoimmune diseases; however, incidents of thromboembolism (TE) precluded further development of these molecules. In this study, we examined the role of the Fc domain interaction with FcγRs in modulating platelet activation and potential for TE. Our results show that the interaction of the 5c8 wild-type IgG1 Fc domain with FcγRs is responsible for platelet activation, as measured by induction of PAC-1 and CD62P. A version of 5c8 with a mutated IgG1 tail was identified that showed minimal FcγR binding and platelet activation while maintaining full binding to CD40L. To address whether Fc effector function is required for immunosuppression, a potent Ab fragment, termed a “domain Ab” (dAb), against murine CD40L was identified and fused to a murine IgG1 Fc domain containing a D265A mutation that lacks Fc effector function. In vitro, this dAb–Fc demonstrated comparable potency to the benchmark mAb MR-1 in inhibiting B cell and dendritic cell activation. Furthermore, the anti-CD40L dAb–Fc exhibited a notable efficacy comparable to MR-1 in various preclinical models, such as keyhole limpet hemocyanin–induced Ab responses, alloantigen-induced T cell proliferation, “heart-to-ear” transplantation, and NZB × NZW F1 spontaneous lupus. Thus, our data show that immunosuppression and TE can be uncoupled and that a CD40L dAb with an inert Fc tail is expected to be efficacious for treating autoimmune diseases, with reduced risk for TE.