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Most academic posts are currently applied for through an online portal called Oriel (www.oriel.nhs.uk). Although it may seem obvious, note that online submission portals are timed down to the second. There is no mercy or defence for late submission – it will not be accepted. Submission of the online application is time consuming, especially if you are applying to more than one academic unit. We would recommend submitting the online application at least 24 hours ahead of the deadline to avoid the fallout of any potential technical meltdown. Also, as a word of caution, you should present your achievements well, but being untruthful is wrong and is a General Medical Council (GMC)-notifiable offence.
The Walport Report in 2005 identified the need to improve the training and fostering of academic clinicians. To this purpose, an Integrated Academic Training Pathway (IATP) was designed – a model that has been adopted in various forms throughout the UK (Figure 1.1). More than a decade later, the Academic Foundation Programme (AFP), Academic Clinical Fellowship (ACF), and Academic Clinical Lectureship (ACL) posts remain fiercely competitive.
In this chapter we will guide you from the beginning to the end of your interview process. We start by giving some advice about preparing for the interview and what to do on arrival at the interview centre. We then discuss how to answer interview questions in general and discuss in detail how to answer the high-yield academic clinical questions. Lastly, we talk about what to expect following the interview and what to do with the result.
It is easy to read this book, think about potential questions and answers, or even write down an answer for every question imaginable. What is difficult, however, is actually saying it out loud. Mock interviews are a key step in your preparation. Think of the interview as a performance and the preparation as the rehearsals.
Our advice would be to have a trusted colleague, ideally, an academic clinician, give you mock interviews. Being asked these questions by and receiving feedback from a colleague who has had the experience of these interviews (either as an applicant or panel member) would be of further gain. Failing that, ask a family member or friend to listen to you. If they are not medical, then this is a good thing, since you will likely also need to make sense to and impress a layperson on the interview panel. As a last resort, if you do not have anyone to practice with, at least practice in front of a mirror!
Choosing which programme to apply for may be a very easy decision, or it may be a fiendishly difficult one. The big question, however, is the same: ‘Where is the best place for you to develop as (a) a clinician and (b) an academic?’ Consideration should be given to both factors.
Being able to defend your person–place–project rationale is key to not only deciding which post to choose from, but also to convince the interview panel that you are a perfect fit for the job. In our opinion, this is the most important aspect of your application and you need to get it nailed down. Everyone is in a different situation, so seek some personal advice from your fellow colleagues and mentors who have experience in academic positions.
Academic clinical posts offer doctors the highly rewarding opportunity to maintain both clinical and research careers, but these opportunities are fiercely competitive. This book provides medical students and doctors-in-training with a complete guide to preparing, applying and interviewing for such posts. Providing guidance on the typical UK academic pathways (including Academic Foundation Programme (AFP), Academic Clinical Fellowship (ACF), and Academic Clinical Lectureship (ACL)), candidates will learn how to choose a programme that suits their needs and experience. They will also get practical tips on how to best showcase their achievements and work portfolio in order to submit the highest quality application. A range of model answers to application and in-person questions are provided, together with a mock interview section demonstrating how to approach tricky questions and interviewers. Prepare for successful academic clinical interviews by following the tips and advice from authors who have excelled at their own interviews.
Understanding the patterns of treatment response is critical for the treatment of patients with schizophrenia; one way to achieve this is through using a longitudinal dynamic process study design.
This study aims to explore the response trajectory of antipsychotics and compare the treatment responses of seven different antipsychotics over 6 weeks in patients with schizoprenia (trial registration: Chinese Clinical Trials Registry Identifier: ChiCTR-TRC-10000934).
Data were collected from a multicentre, randomised open-label clinical trial. Patients were evaluated with the Positive and Negative Syndrome Scale (PANSS) at baseline and follow-up at weeks 2, 4 and 6. Trajectory groups were classified by the method of k-means cluster modelling for longitudinal data. Trajectory analyses were also employed for the seven antipsychotic groups.
The early treatment response trajectories were classified into a high-trajectory group of better responders and a low-trajectory group of worse responders. The results of trajectory analysis showed differences compared with the classification method characterised by a 50% reduction in PANSS scores at week 6. A total of 349 patients were inconsistently grouped by the two methods, with a significant difference in the composition ratio of treatment response groups using these two methods (χ2 = 43.37, P < 0.001). There was no differential contribution of high- and low trajectories to different drugs (χ2 = 12.52, P = 0.051); olanzapine and risperidone, which had a larger proportion in the >50% reduction at week 6, performed better than aripiprazole, quetiapine, ziprasidone and perphenazine.
The trajectory analysis of treatment response to schizophrenia revealed two distinct trajectories. Comparing the treatment responses to different antipsychotics through longitudinal analysis may offer a new perspective for evaluating antipsychotics.
The risk of environmental contamination by severe acute respiratory coronavirus virus 2 (SARS-CoV-2) in the intensive care unit (ICU) is unclear. We evaluated the extent of environmental contamination in the ICU and correlated this with patient and disease factors, including the impact of different ventilatory modalities.
In this observational study, surface environmental samples collected from ICU patient rooms and common areas were tested for SARS-CoV-2 by polymerase chain reaction (PCR). Select samples from the common area were tested by cell culture. Clinical data were collected and correlated to the presence of environmental contamination. Results were compared to historical data from a previous study in general wards.
In total, 200 samples from 20 patient rooms and 75 samples from common areas and the staff pantry were tested. The results showed that 14 rooms had at least 1 site contaminated, with an overall contamination rate of 14% (28 of 200 samples). Environmental contamination was not associated with day of illness, ventilatory mode, aerosol-generating procedures, or viral load. The frequency of environmental contamination was lower in the ICU than in general ward rooms. Eight samples from the common area were positive, though all were negative on cell culture.
Environmental contamination in the ICU was lower than in the general wards. The use of mechanical ventilation or high-flow nasal oxygen was not associated with greater surface contamination, supporting their use and safety from an infection control perspective. Transmission risk via environmental surfaces in the ICUs is likely to be low. Nonetheless, infection control practices should be strictly reinforced, and transmission risk via droplet or airborne spread remains.
Data on average iodine requirements for the Chinese population are limited following implementation of long-term universal salt iodisation. We explored the minimum iodine requirements of young adults in China using a balance experiment and the ‘iodine overflow’ hypothesis proposed by our team. Sixty healthy young adults were enrolled to consume a sequential experimental diet containing low, medium and high levels of iodine (about 20, 40 and 60 μg/d, respectively). Each dose was consumed for 4 d, and daily iodine intake, excretion and retention were assessed. All participants were in negative iodine balance throughout the study. Iodine intake, excretion and retention differed among the three iodine levels (P < 0·01 for all groups). The zero-iodine balance derived from a random effect model indicated a mean iodine intake of 102 μg/d, but poor correlation coefficients between observed and predicted iodine excretion (r 0·538 for μg/d data) and retention (r 0·304 for μg/d data). As iodine intake increased from medium to high, all of the increased iodine was excreted (‘overflow’) through urine and faeces by males, and 89·5 % was excreted by females. Although the high iodine level (63·4 μg/d) might be adequate in males, the corresponding level of 61·6 μg/d in females did not meet optimal requirements. Our findings indicate that a daily iodine intake of approximately half the current recommended nutrient intake (120 μg/d) may satisfy the minimum iodine requirements of young male adults in China, while a similar level is insufficient for females based on the ‘iodine overflow’ hypothesis.
Prion diseases, or Transmissible Spongiform Encephalopathies (TSEs), are a group of fatal neurodegenerative disorders associated with a conformational transformation of the cellular prion protein (PrPC) into a self-feplicating and proteinase K (PK)-resistant conformer, scrapie PrP (PrPSc). Aggregates of PrPSc around neurons lead to neuropathologyical change including neuronal loss, astrogliosis, spongiform degeneration and deposition of amyloid plaques. Currently no effective treatment for prion disease exists. The development of novel therapeutic strategies against prion diseases has become a priority. Several reports have demonstrated that passive and active immune-based therapy can significantly prolong the incubation period of prionoses in vivo, and also some anti-PrP monoclonal can prevent PrP peptide toxicity in vitro. In this study, we have first time identified and purified anti-PrP antibodies from human intravenous immunoglobulin (IVIG) by using PrP peptide affinity chromatography column. The ratio of anti-PrP antibody and IVIG is about 1:1200. In vitro study indicates these anti-PrP antibodies strongly block PrP A117V peptide fibril formation and disrupt formation of fibrillar structures. Furthermore, these antibodies almost completely prevented neurotoxicity of PrP A117V peptide in cultured rat cerebellar granule neuron cultures (CGN). In contrast, immunoglobulins depleted of anti-PrP antibodies had little effect on PrP fibril formation or protection of neuronal cells. Our study suggests that human anti-PrP antibodies may interfere with the pathogenesis of prion disease and these purified antibodies may be a potential therapeutic agent to prevent or slow prion disease progression.