Treatment resistant schizophrenia (TRS) is one of the most disabling of psychiatric disorders, affecting about 1/3 of patients. First-line treatments include both atypical and typical antipsychotics. The original atypical, clozapine, is a final option, and although it has been shown to be the only effective treatment for TRS, many patients do not respond well to clozapine. Clozapine use is related to adverse events, most notably agranulocytosis, a potentially fatal blood disorder which affects about 1% of those prescribed clozapine and requires regular blood monitoring. This as a barrier to prescription and there is a long delay in access for TRS patients, of five or more years, from first antipsychotic prescription. Better tools to predict treatment resistance and to identify risk of adverse events would allow faster and safer access to clozapine for patients who are likely to benefit from it. The CRESTAR project (www.crestar-project.eu) is a European Framework 7 collaborative project that aims to develop tools to predict i) treatment response, particularly patients who are less likely to respond to usual antipsychotics, indicating treatment with clozapine as early as possible, ii) patients who are at high or low risk of adverse events and side effects, iii) extreme TRS patients so that they can be stratified in clinical trials for novel treatments. CRESTAR has addressed these questions by examining genome-wide association data, genome sequence, epigenetic biomarkers and epidemiological data in European patient cohorts characterized for treatment response, and adverse drug reaction using data from clozapine therapeutic drug monitoring and linked National population medical and pharmacy databases, to identify predictive factors. In parallel CRESTAR will perform health economic research on potential benefits, and ethics and patient-centred research with stakeholders.

To date, Ireland has been a leading light in the provision of youth mental health services. However, cognisant of the efforts of governmental and non-governmental agencies working in youth mental health, there is much to be done. Barriers into care as well as discontinuity of care across the spectrum of services remain key challenges. This editorial provides guidance for the next stage of development in youth mental care and support that will require significant national engagement and resource investment.

An unlinked anonymous study was conducted to estimate the prevalence of hepatitis C virus (HCV) infection in emergency department (ED) attendees at a London Hospital. Nine hundred and ninety-seven samples collected over a 12-day period were tested for HCV antibody (Ab) and reactive samples were further tested for HCV RNA. The HCV seroprevalence was 2·6% (26/997) with 1·2% (12/997) HCV RNA positive. A peak HCV RNA-positive prevalence of 4·8% (3/63) was found in males aged 35–44 years, this was compared to 0% (0/136) in males aged <35 years (P = 0·0614) and 1·4% (4/278) in males aged ⩾45 years (P = 0·2415). Assuming the cost for HCV Ab is £6 and HCV RNA is £40 per test, screening ED attendees aged 25–54 years would cost £360 per viraemic infection and identify 82% of those who were HCV RNA positive, yielding the most favourable cost/benefit ratio. HCV screening of ED attendees aged 25–54 years in this population could be an effective way of identifying patients and limit onward transmission.

Extended abstract of a paper presented at Microscopy and Microanalysis 2012 in Phoenix, Arizona, USA, July 29 – August 2, 2012.

The ability to design a diagnostics platform that can achieve cellular level as well as molecular level classification of targeted biomarkers may be critical toward understanding the fundamental basis of disease initiation and proliferation in breast cancer. In this context, we have looked at breast cancer diagnostics and present the design of a biomedical microdevice for evaluating and classifying cellular samples based on their risk towards metastasis. Primary breast cancer tumors have been shown to contain heterogeneous populations of neoplastic cells. Recent studies have demonstrated that subpopulations of these cells can cooperate in the initiation of collective invasion and metastasis. The role of the sensor we present is to identify the type of cells as non-invasive/”follower” cells that do not result in metastasis or invasive “leader” cells that are thought to be responsible for metastasis, from breast cancer cell lysate samples, thus enabling more selective classification of samples, with the eventual goal of early diagnosis. The device is an electrical immunoassay that incorporates the PDGF- receptor to screen the cell lysate samples for the PGDF binding protein that is preferentially expressed in the invasive, “leader” cells. The sensor comprises of alumina nanochannel arrays integrated on to a microelectronic platform operating on the principle of electrochemical impedance spectroscopy to quantify the PGDF protein from the cell lysates.

Differences in reported hand hygiene compliance rates were assessed on the basis of the unit affiliation of observers. In 2 hospitals, unit-based observers more often reported higher compliance rates than did non-unit-based observers (79% vs 58.6%; difference, 20.4%; P<.001). Nonstandardized data collection methods contribute to the variability in hand hygiene compliance rates.

1. A new semi-dominant gene called shaven (Sha) causes hairlessness in the mouse and it is closely linked to naked. Homozygous shaven mice never grow a first coat and adults grow a few short hairs only. Shaven heterozygotes grow a full coat which is greasy.

2. The percentage recombination between shaven and naked was found to be 0·8%. Three-point tests with naked and caracul showed that the order of the three loci is either N–Sha–Ca or N–Ca–Sha.

3. The failure of homozygous shaven mice to grow a coat is due to abnormal keratinization of the hairs in the follicles. The follicles were found to be deficient in sulphydryl groups.

4. The greasiness of the Sha+ coat is due to the presence of a sudanophilic fluid in the hair medullae.

5. The close linkage between the two genes with similar phenotypic effects is discussed.